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101 [ed. note: These data disagree on the presence of NMDA receptors in the soma. For a full description of the properties of NMDA receptors in CA3 pyramidal neurons, please see the apical dendritic compartments.] Recordings from membrane patches of dendrites and soma reveal fast and slow responses to fast application of glutamate, mediated by AMPA amd NMDA receptors, respectively
102 [ed. note: we are not aware of glutamatergic synapses onto the soma] Recordings from membrane patches of dendrites and soma reveal fast and slow responses to fast application of glutamate, mediated by AMPA amd NMDA receptors, respectively
103 1990) causing hyperpolarization, and presynaptic GABAb receptors causing enhancement of synaptic inhibition (Cameron and Williams, 1993). (Reviewed in
104 2 types: one is a slow I AHP type current; weak in LGN, strong in peritenial; the other is fast.
105 5-HT excites 5-HT2 receptors in interneurons and 5-HT1C receptors in pyramidal neurons
106 5HT increases excitability and input resistance
107 90% of cat brainstem input to LGN is cholinergic
108 A 40-50% reduction in a small fraction of (peri-) somatic synapses with large or complex postsynaptic structure after kindling has been found. This functionally relevant reduction may be related to the loss of a specific class of interneurons, and could underlie the enhanced seizure susceptibility after kindling epileptogenesis
109 A combined in situ hybridization and immunocytochemical study demonstrated that Kv1.2 (which may correspond to I(K) channels) is concentrated in the dendrites of CA3 neurons
110 A combined in situ hybridization and immunocytochemical study demonstrated that Kv1.2 (which probably corresponds to I(K) channels) is concentrated in the dendrites of CA3 neurons
111 A D-type potassium current is involved in dendritic calcium spikes initiation and repolarization
112 A distinction was made between axon-bearing and axon-lacking dendrites.
113 a fast voltage activated potassium current that generates the afterhyperpolarization following a fast spike." (data from
114 A linear increase has been found (9 pA/100um) in the density of these channels with distance from soma. It was suggested that this generates site independence of EPSP time course
115 A long duration component of the spike afterhyperpolarization determined the period of the oscillation and was generated by an apamin-sensitive calcium-activated potassium current..”
116 A non-inactivating, Ca-independent, K+ current may limit the amplitude of membrane depolarizations associated with prolonged excursions into the depolarized state
117 A persistent sodium current was the source of current during the depolarizing phase of the oscillation.”
118 A shift toward more depolarized potentials of the activation curve has also been observed in mid and distal dendrites (more than 100um)
119 A single-electrode voltage-clamp technique was employed on slices to examine slow AHP. This was achieved by using conventional procedures to evoke an AHP in current clamp, followed rapidly by a switch into voltage clamp (hybrid clamp). The AHP current showed a dependence on extracellular K+ close to that predicted by the Nernst equation. It could be blocked by Cd2+ or norepinephrine, showed a requirement for voltage-dependent Ca2+ entry, but did not show any clear intrinsic voltage dependence. Once activated, AHP current is not turned off by hyperpolarizing the membrane potential
120 A slow, noninactivating current may have a role to define the limits on the depolarized state, and to govern the spike discharge characteristics once the depolarized state has been reached
121 A slowly activating, outward rectifying potassium current is present in subpopulation of isolated bipolar cells
122 A slowly inactivating A current has also been studied
123 A study in rat using two-photon microscopy to image calcium transients revealed these channels and suggested a novel mechanism for regulation of lateral inhibition
124 A study indicates that synaptic activation of these receptors increases inhibitory activity in relay neurons by increasing output of presynaptic dendrites
125 A study using simultaneous intracellular recording from interneurons and pyramidal neurons combined with biocytin cell fills and morphological reconstructions revealed that the interneurons made connections onto the soma and proximal dendrites of the pyramidal neuron and that stimulation of the interneurons evoked IPSPs in the pyramidal neurons. EM microscopy revealed differential numbers of terminals depending on the subcellular locus of the connections.
126 A subpopulation of interneurons in layer III of the rat piriform cortex are excited by 5-hydroxytryptamine (5-HT) via 5-HT2A receptors and by norepinephrine via alpha 1-adrenoceptors.
127 A subsequent study in rat slice cultures has shown that bath application of MCPG (a mGluR antagonist) blocks the inward Ca-dependent K-current associated with ACPD application or mossy fiber stimulation in the presence on ionotropic GluR antagonists
128 A-channel regulate timing of dendrodendritic inhibition between Mitral cells and granule cells
129 A-channel regulates timing of dendrodendritic inhibition between mitral and granule cells: The transient IA attenuates dendrodendritic input mediated by fast-acting AMPA receptors, such that the excitation and subsequent inhibitory output of granule cells follows the prolonged kinetics of their NMDA receptors. Altering weights of AMPA and NMDA inputs by modulating IA provides a mechanism to regulate the timing of inhibition. A-channels are localized in dendrites.
130 A-channel regulates timing of dendrodendritic inhibition between mitral and granule cells: The transient IA attenuates dendrodendritic input mediated by fast-acting AMPA receptors, such that the excitation and subsequent inhibitory output of granule cells follows the prolonged kinetics of their NMDA receptors. Altering weights of AMPA and NMDA inputs by modulating IA provides a mechanism to regulate the timing of inhibition. A-channels are localized in dendrites.
131 A-current is reduced in the presence of amyloid-beta
132 acetylcholine receptors.
133 Ach exerted two distinct effects on fast-spiking interneurons: Ach directly depolarized FS interneurons by acting on nondesensitizing soma-dendritic nicotinic receptors. In addition, Ach attenuated the GABAergic inhibition of projection neurons by fast-spiking interneurons through activation of presynaptic muscarinic receptors
134 Achergic neurons are in direct synaptic contact with dopaminergic axons in the rat neostriatum
135 Action potential-evoked Ca2+ signals in spines of basal dendrites decreased slightly with distance from the soma
136 action potential-mediated depolarization can...result in the elevation of dendritic intracellular Ca concentration (Regehr et al 1989,
137 Activation curve was studied using patch clamp recordings
138 Activation of both D1- and D2-class receptors has been shown to modulate potassium and sodium currents in acutely isolated neostriatal neurons
139 Activation of M2-class muscarinic receptors in cholinergic interneurons reduces N- and P-type Ca2+ currents through a membrane-delimited pathway using a Gi/o-class G-protein
140 Activation of mGluR increases GC excitability, an effect that should increase GC-mediated GABAergic inhibition of mitral cells
141 Activation of mGluR1 in Purkinje cells causes a Ca-dependent release of a retrograde messenger, probably Glutamate, which acts on presynaptic ionotropic glutamatergic receptor (AMPA/kinate) on the parallel fibers (PFs), depolarizes PFs and modulates neurotransmission from parellel fibers to Purkinje cells
142 Activation of mGluR5 increases GC excitability, an effect that should increase GC-mediated GABAergic inhibition of mitral cells
143 Activation of muscarinic receptors decreases granule cell firing frequency, as well as modulates GABAergic synaptic inputs onto mitral cells.
144 Activation of the adenosine A1 receptor reduces synaptic strength by modulating presynaptic calcium channels. Baclofen modulates presynaptic calcium channels as well but also affects release processes downstream from calcium entry
145 Activation of the Ca2+ current by depolarization as short as 15 ms in a single bipolar cell evokes the glutamatergic postsynaptic currents, of both both NMDA and non-NMDA types, in the Ganglion cells
146 acts on D2 autoreceptors
147 All Calcium Currents. Low Voltage Activated current increased during development
148 All levels of the apical dendrites receive input from granule cells (which receive their input from mossy fibers); the terminals make small spherical vesicle (ss) synapses
149 also in giant cells, and they interact with each other; SOBiv p135). Cartwheel cells are the second most numerous cell in the DCN, after the granule cells (SOBiv p135).
150 Although both the soma and distal dendrites have both the fast and slow GABAA-mediated IPSCs, there is a greater proportion of slow component in the dendrites. Slow GABAA mediated IPSC component is regulated by presynaptic GABAB inhibition (at the interneuron terminals?) whereas the fast is not
151 AMPA and NMDA receptor mediated cortical glutamatergic inputs that were relatively weak compared to the inputs of SPNs and GABAA receptor mediated inhibitory inputs comparable to those of SPNs.”
152 AMPA and NMDA receptors are clustered, and colocalized, on granule cells dendritic spines.
153 AMPA receptors during development: granule cells express a heterogeneous population of AMPA receptors, a subset of which are segregated to postsynaptic sites after synaptogenesis
154 AMPA receptors postsynaptic to the auditory nerve have relatively fast decay kinetics
155 Amplitudes of excitatory postsynaptic conductances (EPSCs) evoked in RTN neurons by minimal stimulation of corticothalamic fibers were 2.4 times larger than in relay neurons, and quantal size of RTN EPSCs was 2.6 times greater. GluR4-receptor subunits labeled at corticothalamic synapses on RTN neurons outnumbered those on relay cells by 3.7 times
156 Amputation of the apical dendrite approximately 30 micron from the soma, while simultaneously recording the slow AHP whole cell current at the soma, depressed the sAHP amplitude by only approximately 30% compared with control. Somatic cell-attached and nucleated patches did not contain sAHP current. Amputation of the axon about 20um from the soma had little effect on the amplitude of the sAHP. By this process of elimination, it is suggested that sAHP channels may be concentrated in the basal dendrites of CA1 pyramids
157 Analysis of synaptic input to layer 4 basket cells show that 79% of symmetric synapses could have originated from other layer 4 basket cells. Soma and proximal dendrites received 76% of all the symmetric synapses
158 Anatomical, electrophysiological and molecular diversity of basket cell-like interneurons in layers II-IV of rat somatosensory cortex were studied using patch-clamp electrodes filled with biocytin
159 and
160 and by cholinergic agonists in slices
161 and can activate Ca action potentials
162 and inside-out membrane patches
163 and it has been shown that nimodipine (an L-channel antagonist) prevents certain mossy fiber LTP-types from taking place
164 and nicotinergic
165 and Shepherd GM ed. Synaptic Organization of the Brain, 1998. p182) GABA release onto mitral: spontaneous and gltamate-evoked. Moreover, activation of muscarinic receptors modulates GABAergic synaptic inputs onto mitral cell.
166 and Shepherd GM ed. Synaptic Organization of the Brain, 1998. p182)GABA release onto mitral: spontaneous and gltamate-evoked. Moreover, activation of muscarinic receptors modulates GABAergic synaptic inputs onto mitral cell.
167 and stain for postsynaptic GLYR
168 Another study suggested that adult neostriatal projection neurons do not express significant levels of LVA Ca2+ current
169 Another study using bath application of 1S,3R-ACPD in rat slice cultures during single electrode voltage clamp recording showed that depolarizing current steps revealed a suppression of K currents leading to a negative slope conductance at potential between -55mV and -40 mV
170 AP propagation was studied in the somas and dendrites of intact retinal ganglion cells exposed by enzymatic removal of the overlying endfeet of the Muller glia. Simultaneous somatic and dendritic whole cell patch recordings suggested that the dendrites of retinal ganglion cells support Na+ AP.
171 Apical dendrites of L6 pyramidal neurons in somatosensory cortex are similar to L5 and L2/3 in that they includeNMDA-dependent electrogenesis
172 Application of acetylcholine (ACh) evoked concentration-dependent whole-cell currents
173 Assumed.
174 At least 40% of choline acetyltransferase-immunopositive cholinergic interneurons were immunopositive for GluR1 or GluR4
175 At parallel fiber (PF) -Purkinje cell synapses, NMDA reversibly depresses postsynaptic currents, through a trans-synaptic mechanism that involves release from PFs nitric oxide that decreases the glutamate sensitivity of the Purkinje cell
176 At the subcellular level in the substantia nigra pars reticulata (SNr), GlyRs show a localized distribution on the soma and dendrites that partially complements but does not overlap with the distribution of gamma-aminobutyric acid (GABA)A receptors."
177 Autaptic self-innervation of basket cells
178 Auto-activation from glutamate released by mitral cell secondary dendrites
179 Auto-activation from glutamate released by mitral cell soma
180 Baclofen suppresses field potentials at the intrinsic fiber synapses proximal to the pyramidal cell bodies (layer Ib) but not field potential at distal dendrites (layer Ia). afferent and intrinsic synaptic inputs may be differentially modulated by the activation of GABAB receptors and that this selective suppression is at least partially mediated via a presynaptic mechanism (at the interneuron terminals?)
181 Basal dendrites receive flattened (FL) and pleiomorphic (PL) synapses (90% of total synapses on proximal dendrites, 62% on distal dendrites) (SOBiv p131). Vertical cells stain for glycine
182 Basket cell activation elicits IPSPs in Purkinje cells
183 Basket cells make synaptic contact with pyramidal and spiny stellate cells preferentially on the somata (50%) and dendritic shaft (45%), but synapses on dendritic spines are also present (4.9%). IPSPs elicited in the postsynaptic cells have short latency, fast rising time and short duration, similar to those mediated by GABAA receptors
184 Bath application of omega-conotoxin MVIIC (an antagonist of N and P channels) blocked (with slow kinetics) approximately 30% of the high-voltage activated Ca2+ current measured in whole-cell recordings
185 Bath application of omega-conotoxin MVIIC blocked (with rapid kinetics) approximately 20% of the high-voltage activated Ca2+ current, suggesting the presence of N-channels measured in whole-cell recordings
186 Bath application of Pb2+ shifted the neurons curent-voltage relation in patch-clamp recording from acutely isolated pyramidal neurons. These results were interpreted to "demonstrate that Pb2+ in micromolar concentration is a voltage-dependent, reversible blocker of delayed-rectifier potassium currents of hippocampal neurons"
187 Bath application of Pb2+ shifted the neurons'' current-voltage relation in patch-clamp recording from acutely isolated pyramidal neurons. These results were interpreted to "demonstrate that Pb2+ in micromolar concentration is a voltage-dependent, reversible blocker of delayed-rectifier potassium currents of hippocampal neurons"
188 Benardo et al 1982;
189 Bicuculline disrupts timing of odor_evoked responses
190 Blockade of fast spike by TTX
191 blocked by strychnine. Ia IPSPs are located near the cell soma
192 Both HVA and LVA calcium currents were present in cell bodies of identified neurons. P/Q-type channels accounted for only 6 % of HVA, while L-, N- and R-type Ca2+ channels each accounted for around one-third of the somatic calcium current.
193 Both ionotropic NMDA and non-NMDA autoreceptors are activated by glutamate released from primary and secondary dendrites. In contrast to non-NMDA autoreceptors, NMDA autoreceptors are almost exclusively located on secondary dendrites and their activation generates a large and sustained self-excitation. Both intracellularly evoked and miniature NMDA-R mediated synaptic potentials are blocked by intracellular BAPTA and result from a calcium-dependent release of glutamate
194 Both X and Y relay neurons receive inputs from TRN axons. The X neurons are innervated both within the glomerulus and above the glomerulus on the middle of the denritic tree (SOBIV p301, 305).
195 but not LTP or LTD (SOBiv p90).
196 but not LTP or LTD (SOBiv p90).Motoneurons have a high density of AMPA receptors (Vandenberghe et al, JNS 20: 7158, 2000). There is evidence that "glutamate receptor-mediated Ca2+ influx, intracellular Ca2+ accumulation, and subsequent cell death" may be involved in the mechanism of selective motoneuron degeneration in amyotrophic lateral sclerosis.
197 but not LTP or LTD (SOBiv p90).Postnatal development and properties of these receptors were studied with whole-cell and outside-out patch-clamp. The conductance and relative distribution were independent of age from postnatal day 4 to 14. The results also suggested that their properties differ from those in spinal cord interneurons
198 but the postsynaptic target is most likely amacrine cells (SOBiv p238).
199 By combining intracellular recordings and two-photon microscopy imaging of [Ca]i in rat it was shown that APs backpropagate at full amplitude up to the tuft
200 By combining intracellular recordings and two-photon microscopy imaging of [Ca]i it was shown that AP propagate at full amplitude up to the most distal branches
201 by contrast,
202 By using dendritic recordings and calcium transients in rats it was shown that this current may control AP propagation in lateral dendrites
203 Ca -dependent Chloride current at the presynaptic terminals of goldfish retinal bipolar cells
204 Ca fluorescence imaging shows that application of L-channel antagonists reduces the Ca influx associated with backpropagating action potentials, and has a significantly greater effect in the proximal dendrites than in more distal dendrites
205 Ca fluorescence imaging shows that application of N-channel antagonists slightly reduces the Ca influx associated with backpropagating action potentials
206 Ca fluorescence imaging shows that application of P-channel antagonists reduces the Ca influx associated with backpropagating action potentials
207 Ca-dependent potassium currents are seen in dissociated cells
208 CA1 neurons and subiculum neurons in hippoampus differ in firing pattern (the former being regular and the later being either regular, weakly bursting or strongly bursting) and resting membrane properties (such as input restistance and membran time constant); however, low concentration of 4-AP (50 &#181M) can convert neurons in both regions into firing bursting action potentials
209 CA1 neurons and subiculum neurons in hippoampus differ in firing pattern (the former being regular and the later being either regular, weakly bursting or strongly bursting) and resting membrane properties (such as input restistance and membran time constant); however, low concentration of 4-AP (50 ?M) can convert neurons in both regions into firing bursting action potentials
210 CA1 neurons and subiculum neurons in hippoampus differ in firing pattern (the former being regular and the later being either regular, weakly bursting or strongly bursting) and resting membrane properties (such as input restistance and membran time constant); however, low concentration of 4-AP (50 µM) can convert neurons in both regions into firing bursting action potentials
211 CA1 pyramidal neurons increase their firing (recorded extracellularly) in response to ionophoresed Glu within their apical dendritic fields or in the cell body layer (Dudar 1974 PMID#4437726).
212 Ca2+ -activated K+ current at presynaptic terminals of goldfish retinal bipolar cells
213 Ca2+-activated K+ currents were studied using whole-cell patch-clamp recordings from freshly dissociated mouse neocortical pyramidal neurons
214 Calcium entry through N-type calcium channels (CaV2.2) causes activation of KCa channels that decrease the firing rate and increase the regularity of firing in SNr GABA neurons”
215 Calcium influx through NMDA receptors can directly trigger presynatic GABA release for local dendrodendritic feedback inhibition. DDI is elicited by photorelease of caged Ca++, with and without Cd++ and Ni++.
216 Calcium influx through NMDA receptors directly evokes GABA release in granule cells.
217 Calcium is involved in delayed release of neurotransmitter at synapses between granule cell their postsynaptic targets (stellate cells and Purkinje cells)
218 Calcium-dependent potassium channels are preferentially activated by calcium entry through N- and Q-type channels
219 CaV channels are among the intrinsic membrane channels influencing the excitability of the SNr neuronal membrane. CaV channels have been shown to influence spontaneous activity in these neurons, as well as more complex behaviors such as plateau potential generation burst firing.”
220 Cell-attached dendritic recordings in rats up to about 60um from the soma showed that low-threshold calcium channels were concentrated at proximal dendritic locations, sites known to receive excitatory synaptic connections from primary afferents, suggesting that they play a key role in the amplification of sensory inputs to TC neurons
221 Cell-attached patches on the proximal 100um of the apical dendrite did not contain sAHP channels. Amputation of the apical dendrite approximately 30 micron from the soma, while simultaneously recording the sAHP whole cell current at the soma, depressed the sAHP amplitude by only approximately 30% compared with control. Somatic cell-attached and nucleated patches did not contain sAHP current. Amputation of the axon about 20um from the soma had little effect on the amplitude of the sAHP. By this process of elimination, it is suggested that sAHP channels may be concentrated in the basal dendrites of CA1 pyramids
222 Cell-attached recordings in rats up to about 60um from the soma demonstrated a non-uniform dendritic distribution of channels
223 Cell-attached recordings in rats up to about 60um from the soma demonstrated a roughly uniform density of channels across the somatodendritic area examined that corresponds to approximately half the average path length of TC neuron dendrites
224 Cell-specifc modulation of GABAA receptor- mediated chloride current by dopamine. In interneurons (mainly granule cells), dopamine reduces GABAA Cl- current, via D1 receptor and involves phosphorylation of GABAA receptors by PKA. In mitral cell, dopamine enhances GABA responses via activation of D2 receptors and phosphorylation of GABAA receptors via PKC.
225 Cell-specifc modulation of GABAA receptor- mediated chloride current by dopamine. In interneurons (mainly granule cells), dopamine reduces GABAA Cl- current, via D1 receptor and involves phosphorylation of GABAA receptors by PKA. In mitral cell, dopamine enhances GABA responses via activation of D2 receptors and phosphorylation of GABAA receptors via PKC.
226 Cells acutely dissociated from slices obtained from chronic temporal lobe epilepsy patients displayed a high-voltage activated Ca2+ conductance with a pronounced Ca2+-dependent inactivation
227 Cells were voltage-clamped using a single microelectrode, at 23-30 degrees C. M-current resembled that of sympathetic ganglion cells. It was abolished by addition of carbachol, muscarine or bethanechol, as well as by 1 mM barium. It was suggested that activation of cholinergic septal inputs to the hippocampus facilitates repetitive firing of pyramidal cells by turning off the M-conductance, without much change in the resting potential of the cell
228 Cerebellar granule cells from young rats (postnatal days 1-9) possess voltage-activated inward Na+ current as well as two types of K+ current, IA and IK
229 Chen et al 1997). Dendritic patch recordings showed an even density of Na channels (120pS um-2) up to 350 um from the soma along the primary dendrite to the origin of the glomerular tuft
230 Chen et al 1997).Dendritic patch recordings showed an even density of Na channels (120pSum-2) up to 350 um from the soma along the primary dendrite to theorigin of the glomerular tuft
231 Choline acetyltransferase immunocytochemistry shows that cholinergic projections from the basal forebrain to the main olfactory bulb focus synaptic innervation on interneurons, on the dendritic spines of periglomerular and granule cells.
232 Cholinergic agonist carbachol caused a significant suppression of inhibitory postsynaptic potentials (IPSPs) in the pyramidal neurons that were induced by stimulation of layer Ib, with a weaker effect on IPSPs induced by stimulation of layer Ia
233 Cholinergic agonist carbachol selectively suppresses intrinsic fiber synaptic potentials but not afferent fiber synaptic potentials.
234 Cholinergic agonist carbachol selectively suppresses intrinsic fiber synaptic potentials but not afferent fiber synaptic potentials. A presynaptic mechanism of cholinergic suppression is suggested
235 Cholinergic agonist carbachol selectively suppresses intrinsic fiber synaptic potentials but not afferent fiber synaptic potentials. (Hasselmo ME and Bower JM, 1992353 ) (Patil MM and Hasselmo ME, 1999341 ).
236 Cholinergic interneurones in rat exhibit a ATP-sensitive potassium channel current. sigle-cell-RT-PCR shows that this channel is formed from Kir6.1 and SUR1 subunits
237 cited in Johnston and Amaral, 1998).
238 Clusters of glycine receptors were found on the somatodendritic membranes of Alpha ganglion cells
239 Clusters of the alpha1, and alpha2, alpha3, and gamma2 subunits of the GABAA receptor were found on the somatodendritic membranes of Alpha ganglion cells. Experiments with different combinations of the subunit-specific antibodies showed that the alpha1, alpha2, and alpha3 subunits of the GABA(A) receptor are not colocalized within the same clusters, suggesting that an individual neuron can express several isoforms of the GABAA receptor and that these different isoforms are aggregated at distinct postsynaptic sites
240 Combining preembedding and postembedding immunostaining at the EM level, GluR2/3 and NMDAR1 immunoreactivity was located in somata and in proximal and distal dendrites
241 Conduction of the action potential suggests there must be some Na channels there.
242 Cultured cells
243 Cultured cells; blocked by 100 uM Cd or nifedipine (IC50=368 nM); no T-type Ca channels found
244 Cultured cells; TTX-sensitive
245 Curare blocks responses to applied ACh.
246 D2 dopamine receptors reduce N-type Ca2+ currents in rat neostriatal cholinergic interneurons
247 D5 and D2 dopamine receptors induce "depolarization and an increase in input resistance in striatal FSI in brain slices"
248 DA is released from dendrites
249 DA receptors in mitral cell dendrites implied by DA localization in PG dendrites presynaptic to mitral dendrites
250 DDI (dendrodendritic inhibition) can be elicited by activation of AMPA receptors, while NMDA receptor activation is not an absolute requirement. DDI is blocked by Cd and toxins to N- and P/Q-type channels.
251 DDI (dendrodendritic inhibition) can be elicited by activation of AMPA receptors, while NMDA receptor activation is not an absolute requirement. DDI is blocked by Cd and toxins to N- and P/Q-type channels.
252 Deep multipolar cells have GABA-containing terminals arranged in baskets around pyramidal cell bodies
253 Delayed firing of action potentials in response to current pulse injection suggests there is I A current here. Unpublished data have characterized the kinetics of A current in the rat mitral cell
254 Delayed rectifier. (See SOBiv p140).
255 Dendritic can fire sodium spikes that can precede somatic action potentials (APs), the probability and amplitude of which depend on previous synaptic and firing history. Some dendritic spikes could occur in the absense of somatic APs, indicating that their propagation to soma is unreliable
256 Dendritic fluorescence imaging showed that Ca2+ channels of several subtypes mediated the AP-evoked fluorescence transient in the proximal (100-170 microns) apical dendrite. The fluorescence resulted from Ca2+ entry through L, N, and P-type channels, and through Ca2+ channels (R-type) not sensitive to L-, N- and P-type Ca2+ channel blockers
257 Dendritic GABAA-mediated IPSPs act largely independent of somatic IPSPs and may regulate facilitation of MNDA-mediated respnses
258 Dendritic patch recordings showed an even density of Na channels (120pS um-2) up to 350 um from the soma along the primary dendrite to the origin of the glomerular tuft
259 Dendritic patch recordings showed an even density of Na channels (120pSum-2) up to 350 um from the soma along the primary dendrite to theorigin of the glomerular tuft
260 Dendrodendritic from granule cell spines. IPSP blocked by bicuculline and low Cl-
261 Dendrodendritic inhibition (DDI) between mitral and granule cells relies on N-and P/Q- type calcium channels. Magnitude of DDI is proportional to dendritic calcium influx.
262 Dendrodendritic inhibition (DDI) between mitral and granule cells relies on N-and P/Q- type calcium channels. Magnitude of DDI is proportional to dendritic calcium influx.
263 Dendrodendritic inhibition between mitral and granule cells involves N-and P/Q- type calcium channels. The magnitude of DDI is proportional to dendritic calcium influx.
264 Dendrodendritic inhibition between mitral and granule cells involves N-and P/Q- type calcium channels. The magnitude of DDI is proportional to dendritic calcium influx.
265 Dendrodendritic synapse onto mitral/tufted cells, of type 2
266 Densities and kinetics were measured from patch clamp recordings
267 Depolarisations beyond -40 mV activated a fast transient TTX-sensitive inward current. Once activated, INa declined exponentially to zero following a single exponential. The underlying conductance showed a sigmoidal activation between -40 and +30 mV, with half activation at -17.4 mV and a maximal value of 9.7 nS per neurone. The steady-state inactivation was complete at -30 mV and completely removed at -90 mV, with a midpoint at -56 mV. The activation process could be adequately described by third order kinetics, with time constants ranging from 260 microseconds at -20 mV to 70 microseconds at +50 mV.
268 Depolarization induced transient outward currents that resembled IPSCs and were blocked by GABA and glycine receptor antagonists, suggesting that they arise from activation of amacrine feedback synapses
269 Depolarizes SNr principle cells. Generated by subset of voltage-gated sodium channels that remain open for extended periods of time. Can contribute to neuronal excitability and pacemaking activities.
270 Depolarizing "sag" during larger hyperpolarizing voltage transients is indicative of Ih current in determinating the passive membrane properties of CA1 pyramidal neurons
271 Different GABAergic receptors are localized to specific layers, and may mediate feedforward and feedback inhibitions
272 Differential GABABergic presynaptic modulation in layers Ia and Ib: While baclofen suppresses field potentials at the intrinsic fiber synapses proximal to the pyramidal cell bodies (layer Ib), it does not affect field potentials at distal dendrites (layer Ia)
273 Differential induction of potentiation and depression at commissural and mossy fiber synapses has also been shown by
274 Differential induction of potentiation and depression at commissural and mossy fiber synapses has also been shown by #R#158#E#. Recordings from membrane patches of dendrites and soma reveal fast and slow responses to fast application of glutamate, mediated by AMPA amd NMDA receptors, respectively
275 discussed in Burke 1998).
276 Dopamine modulates Ih in cultured rat olfactory receptor neurons
277 Dopaminergic afferents from substantia nigra pars compacta” target the globus pallidus.
278 Dopaminergic subdivision of the periglomerular interneurons throughout classes of vertebrates.
279 Dual patch recordings and Ca2+ imaging of mitral cells in the rat olfactory bulb slice suggested that action potentials propagating into the basal dendrites decrement approximately 20% per 100um
280 Dual patch recordings and Ca2+ imaging of mitral cells in the ratolfactory bulb slice suggested that action potentials propagating intothe basal dendrites decrement approximately 20% per 100um
281 Dual patch-clamp recordings showed that Ca-activated K+ (BK) channels were not triggered by neuronal action potentials in normal slices and only opened as neuronal responses deteriorated (smaller or absent spikes) and in a spike-independent manner, suggesting that BK channels may activate only in pathological conditions
282 Dual recording from pyramidal cell-basket cell pairs reveal unitary EPSPs in basket cells mediated by one and two synaptic junctions. The unitary EPSPs have fast rising time and short time duration. Closely timed (10-50 ms) pairs of presynaptic action potentials resulted in statistically significant paired-pulse depression. The reliability of transmission is high, but the fast time course of the EPSPs constrains their temporal summation. Due to the relatively small amplitude of unitary EPSPs several convergent inputs will therefore be required to elicit suprathreshold responses.
283 Dual whole-cell recordings in acute slices showed that kainate receptors located on presynaptic interneuron terminals can be activated by glutamate released from the somatodendritic compartment of the postsynaptic pyramidal cells
284 Dual whole-cell recordings in connected cell pairs suggested that attenuation of local horizontal excitation by dopamine is through D1 actions at a presynaptic site
285 Dual whole-cell recordings showed that Ca2+-dependent release of a retrograde messenger, most probably glutamate, from dendrites suppresses the inhibition of pyramidal neurons
286 During periods of induced regular firing, intrastriatal stimuli were used to evoke pharmacologically isolated monosynaptic AMPA receptor-mediated EPSPs or GABAA receptor-mediated IPSPs. EPSPs evoked during the interspike interval (ISI) produced a phase-dependent decrease in the ISI, whereas IPSPs produced a phase-independent prolongation of the ISI
287 Each isoform [of Na channel] was found within neuronal somata and dendrites of all diameters within the GP".
288 Effects of odorants on this current in newt ORNs were investigated using whole-cell patch-clamp
289 Electrophysiological classification of juxtaglomerular neurons: bursting and standard firing. In contrast to the standard firing neurons, bursting neurons produced a calcium-channel-dependent low-threshold spike (LTS) when depolarized either by current injection or by spontaneous or evoked postsynaptic potentials. Bursting neurons also could oscillate spontaneously. Most bursting cells were either periglomerular cells or external tufted cells. Based on their mode of firing and placement in the bulb circuit, these bursting cells are well situated to drive synchronous oscillations in the olfactory bulb. LVA (low voltage-activated) Ca++ channel may be involved in LTS.
290 Electrophysiological evidence shows that N-channels and L-channels are present in all dendritic compartments in turtle motoneurons
291 Electrophysiology data: AP5 attenuates delayed excitatory components in peristimulus time histograms of mitral cell unit responses to olfactory nerve volleys
292 Electrophysiology data: DNQX attenuates early and late excitatory components in peristimulus time histograms of mitral cell unit responses to olfactory nerve volleys
293 EM evidence for GABAergic input to deeper dendritic layers
294 EM showed colocalization at axodendritic asymmetric synapses within the CA1 subfield of rat hippocampus. AMPA/NMDA receptor colocalization was found in non-GABAergic dendritic shafts as well as dendritic spines, suggesting that excitatory neuronal transmission in CA1 neurons may generally involve activation of both NMDA and AMPA receptor subunits at a single synapse
295 Estimated: HH model slightly modified from
296 Estimated: HH model slightly modified from Traub, 1982
297 Evidence from intracellular responses to nicotine, but not to oxotremorine
298 Evidence of presence of high-threshold calcium channel
299 Evidence of spatial and temporal facilitation of fast IPSPs, interpretated as the convergence of excitatory input onto the inhititory interneurons from different olfactory structures
300 Experimental findings support a cascade for induction of homosynaptic, NO-dependent LTD involving activation of guanylyl cyclase, production of guanosine 3',5' cyclic monophosphate and subsequent PKG activation. This process has an additional requirement for release of Ca2+ from ryanodine-sensitive stores
301 Extracelluar ACPD (an mGluR agonist) application to apical or basal dendrites of CA1 pyramidal neurons causes local increases in calcium concentration that propagate throughout the cell, as measured by simultaneous whole cell recording and confocal microscopy with calcium imaging
302 Extracellular recordings in vivo suggested that the dendritic density of these channels rapidly decreases with distance from soma
303 Fast IPSP, blocked by bicuculline and low Cl-
304 for review see Llinas and Walton 1998).
305 found an NMDA component in neonatal rat. Short-term post-tetanic potentiation (PTP) and depression (PTD) occur
306 found evidence for the presence of GABAB receptors on cell dendrites. Recordings in slices showed that GABA inhibition was mediated by GABA(B) receptors in the dendrites and GABA(A) receptors in the soma and dendrites. Therefore, the GABA released by stellate cells modulates Purkinje cells activity through two inhibitory mechanisms
307 From cerebral cortex
308 From rodents to primates, the SNr and GPi innervate thalamic and brain stem nuclei connected to motor, prefrontal, parietal and temporal associative cortical areas offering an access for BG to control motor, cognitive, as well as emotional–motivational processes.”
309 FSIs “have GABAergic inputs originating from the GP. The pallidostriatal inputs are largely selective for FSIs (Bevan et al., 1998) and in vivo, increased firing of FSI during choice selection in a simple discrimination task coincide with a decrease in firing of GP neurons .”
310 GABA and glycine conductances of isolated bipolar cells
311 Gaba being from Amacrine Cells
312 GABA from basket cell inhibitory interneurons.
313 GABA from chandelier inhibitory interneurons.
314 GABA from some Renshaw interneurons; IPSPs are Cl- mediated, potentially blocked by picrotoxin
315 GABA inactivation of large-basket cells of visual cortex resulted in weakened orientation and direction selectivity, via weakening of long-range lateral inhibition by the basket cells
316 GABA is a neurotransmitter used by basket cells or clutch cells
317 GABA is the transmitter released from large superficial horizontal cells and small globular-soma cells which mediate feed-forward inhibition of the pyramidal neurons when activated by axon terminals of mitral/tufted cells in the lateral olfactory tract or association fibers from other pyramidal neurons
318 GABA(A) and GABA(C) receptor-mediated currents were observed in the isolated terminal
319 GABA(A) receptors mediate GABAergic inhibition on bipolar cell dendrites in the OPL, that GABA(A) and GABA(C) receptors mediate inhibition on axon terminals in the IPL, and that the GABA(C):GABA(A) on the terminals may tune the response characteristics of the bipolar cell
320 GABA(A)-mediated (bicuculline-sensitive) inhibitory responses can be demonstrated in CA1 neurons by extracellular recording (Curtis et al, 1970) and by recording spontaneous synaptic currents (Collingridge, 1984).
321 GABAB receptors act presinaptically to regulate the release of glutamate from olfactory nerve terminal
322 GABAergic inhibitory synapses onto mitral cells, through dendrodendritic spine synapse: possibly two types: self inhibition and lateral inhibition.
323 GABAergic interneurons (basket cells, dendrite-targeting cells, and double-bouquet cells) form reciprocally interconnected intracortical networks in which basket cells play a prominent role, given the strength of innervation and the proximal placement of synapses by basket cells to their postsynaptic targets
324 GABAergic interneurons in deeper layers of piriform cortex receive symmetric synapses as well as asymmetric synapses
325 GABAergic responses evoked by electrical stimulations have been studied in slices
326 GABAergic synaptic inputs originating from the globus pallidus were also demonstrated ultrastructurally using juxtacellular labeling and NOS immunocytochemistry.”
327 GAD-positive gemmules (spines) of granule cells were observed to form reciprocal dendrodentritic synaptic junctions with mitral cell dentrites which lacked reaction product.
328 GAD-positive staining
329 GAD-positive staining gemmules (i.e., spines) of periglomerular cells also formed reciprocal dendrodentritic synaptic contacts with mitral/tufted cell dentrites.
330 GLU acts on both AMPA and NMDA receptors
331 Glu from Ia axon terminals (reviewed in
332 GLU is the primary excitatory transmitter of association fiber terminals
333 GLU is the primary excitatory transmitter of the afferent fiber terminal of mitral and tufted cells
334 Glutamate - kainate receptor (glur6)In mouse hippocampal slices, bath application of kainate caused presynaptic reduction in epscs at mossy fiber synapses on CA3 pyramidal cells in glur6 knockouts but not in glur5 knockouts.
335 Glutamate is commonly believed to be the primary excitatory neurotransmitter in the hippocampal formation generally (reviewed in Cotman et al., 1995), and in CA1 in particular
336 Glutamate is released from Ia terminals
337 Glutamate release from parallel fibers (of granule cells) activates AMPA, mGluR on Purkinje cells
338 Glutamatergic fibers originated in the subthalamic nucleus and, to a lesser extent, in the cerebral cortex and thalamus” target the globus pallidus.
339 GLY ionophoresis mimics Ia IPSPs (reviewed by
340 Glycine and GABA elicit concentration-dependent desensitizing currents mediated by chloride.
341 Glycine and GABA exert inhibitory actions on olfactory bulb neurons, mitral/tufted cells, granule and periglomerular cells).
342 Glycine from some Renshaw interneurons; IPSPs are Cl- mediated, potentially blocked by strychnine
343 granule cell dendrodendritic synapses:
344 granule cells are GABAergic:
345 Granule cells compensate for the lack GABAA receptors (in somatic location? ) by expressing the two-pore-domain K+ channel TASK-1, a voltage-independent K + conductance so as to maintain normal neuronal behaviour; this finding highlight the importance of GABAA receptor-mediated background inhibition
346 Granule cells that lack GABAA receptors (in somatic location? ) express the two-pore-domain K+ channel TASK-1, a voltage-independent K + conductance, so as to maintain normal neuronal behaviour
347 Group III mGluRs mediate a direct suppression of bipolar cell transmitter release, through a mechanism of presynaptic autoreceptors
348 Half of the cells from the study
349 have glycine receptors.
350 have provided evidence for active properties. Dual patch recordings show backpropagating impulses
351 High concentration of NE acts at Alpha1 receptors to increase GC excitability and increase GABAergic inhibition inhibition of MC
352 High concentration of NE acts at Alpha2 receptors to decrease GC excitability and decrease GABAergic inhibition inhibition of MC
353 High-voltage-activated (HVA) and low-voltage-activated (LVA) Ca2+ currents were observed in the isolated rod bipolar cell terminal recordings
354 Hilar stimulation has been used to elicit (pharmacologically isolated) IPSPs in CA3 pyramidal neurons (recorded by means of intracellular or whole cell methods depending on the age of the animal). Paired pulse stimulation in this preparation resulted in paired pulse depression, which could be reduced by bath application of CGP35348 (a GABA(B)R antagonist) in adult rats. Neonatal rats (5-7 days old) showed paired pulse depression only within a much shorter range of interstimulus intervals and it was not affected by CGP35348 unless transmitter release was facilitated by raising the bath [Ca2+] and lowering the bath [Mg+]
355 Histochemical studies have established that SNr receivesdense 5-HT innervation originating from 5-HT neurons inraphe nuclei.”
356 histological experiments found Ih expressed in many olfactory bulb cell types including periglomerular cells.
357 histology experiments found Ih in granule cells.
358 Horizontal cells in layer Ia are labelled for GAD and GABA, but not for GABA takeup, suggesting lack of local axon collaterals or high-affinity GABA takeup sites
359 However, channel density varied widely in the proximal compartment, possibly indicating the presence of hot spots.
360 However, in a few apical patches the channel density was increased X 3, which could indicate channel clustering. Ca fluorescence imaging shows that application of T-channel antagonists reduces the Ca influx associated with backpropagating action potentials, and has a two-fold greater effect in the dendrites than in the soma
361 However, in a few apical patches the channel density was increased X 3, which could indicate channel clustering. Ca fluorescence imaging shows that application of T-channel antagonists reduces the Ca influx associated with backpropagating action potentials, and has a two-fold greater effect in the dendrites than in the soma
362 However, in a few apical patches the channel density was increased X 3, which could indicate channel clustering. Ca fluorescence imaging shows that application of T-channel antagonists reduces the Ca influx associated with backpropagating action potentials, and has a two-fold greater effect in the soma than in the dendrites
363 However, in guinea pigs, a combination of high-speed imaging and simultaneous intracellular recordings showed that direct depolarization of the soma or dendrites never caused dendritic [Na+]i increases, suggesting that the climbing fiber-activated [Na+]i changes in the dendrites are due to Na+ entry through ligand-gated channels
364 However, recordings in slices showed that D1 receptor activation can either inhibit or enhance evoked activity, depending on the level of membrane depolarization, by modulating an L-type Ca2+ conductance
365 I M may contribute to a sag and rebound of voltage response to hyperpolarizing current steps
366 Ia EPSPs are mediated largely by AMPA receptors (muscle afferents:
367 Ia IPSPs are chloride mediated
368 Ia IPSPs are readily affected by soma current or Cl- injection, indicating location at the soma or proximal dendrites
369 Ia synapses are immunoreactive for GLU
370 Identification of subunit mRNAs
371 Ih conductance causes voltage attunuation and is more concentrated in dendrites than in soma
372 Ih current: slowly developing hyperpolarisation-activated current with a threshold generally positive to resting potential and with a strongly voltage-dependent activation time constant. The current was Na+- and K+-sensitive, suppressed by external Cs+, and insensitive to Ba++. The Ih should be tonically active at rest, and may contribute to the oscillatory behaviour of the bulbar network
373 Immunochemical evidence of glutamate as neurotransmitter in the terminals of parallel fibers
374 Immunocytochemistry and in situ hybridisation showed that NMDAR1 was expressed in most CN neuronal types, including the fusiform cell apical dendrites. However, fusiform cell basal dendrites, which are the synaptic sites of cochlear nerve fibers, did not express NMDAR1
375 Immunohistochemical evidence shows that CaV1.3 (an L type channel; seeMembrane Properties Resource) is present in soma and all dendritic compartments in turtle motoneurons
376 Immunohistochemical evidence shows that CaV1.3 is present in soma and all dendritic compartments in turtle motoneurons
377 Immunolabeling was observed in soma and dendrites of layer V pyramidal cells in the frontal cortex
378 Implied by current clamp recording of action potential at soma
379 Implied by data on more proximal dendritic regions; still to be tested
380 Implied by Glu released by other compartments of the mitral cell (Dale's law). Target (destination) is presumably PG cell dendrites in the glomerulus
381 Implied by recording of fast prepotential. Dual patch recordings provide evidence for both backpropagating and forward-propagating impulses in the primary dendrite
382 Implied from evidence that local interneurons colocalize FMRFamide and GABA
383 Importance for membrane excitability of an GABAB receptor-activated inward-rectifying potassium current, sensitive to pertussis toxin and barium
384 In a study of acutely isolated rat cells under whole cell recording across development states (Day 6 - Day 29), it was found that delayed rectifier currents decayed along a double-exponential time course and were 50% blocked by TEA (tetraethylammonium, a I(K) antagonist) at +30 mV at a concentration of about 1mM, as well as being partially blocked by 4-AP (4-aminopyridine). The current also appeared to increase over this development period. This increase was approximately 300% much larger in CA1 cells than in CA3 cells, with only approximately 50%
385 In a study of acutely isolated rat cells under whole cell recording across development states (Day 6 - Day 29), it was found that delayed rectifier currents decayed along a double-exponential time course and were 50% blocked by TEA (tetraethylammonium, a K(DR) antagonist) at +30 mV at a concentration of about 1mM, as well as being partially blocked by 4-AP (4-aminopyridine). The current also appeared to increase over this development period. This increase was approximately 300% much larger in CA1 cells than in CA3 cells, with only approximately 50%
386 In a study of acutely isolated rat cells under whole cell recording across development states (Day 6 - Day 29), it was found that delayed rectifier currents decayed along a double-exponential time course and were 50% blocked by TEA (tetraethylammonium, a K(DR) antagonist) at +30 mV at a concentration of about 1mM, as well as being partially blocked by 4-AP (4-aminopyridine). The current also appeared to increase over this development period. This increase was approximately 300% much larger in CA1 cells than in CA3 cells, with only approximately 50%
387 In a study of acutely isolated rat cells under whole cell recording across developmental states (Day 6 - Day 29), I(A) was separated from I(K) by subtraction methods. It was found that I(A) was rapidly activated and inactivated and was 80% blocked by 4-AP (4-aminopyridine), but was insensitive to TEA (tetraethylammonium) and dendrotoxin (Klee et al, 1995). The current has also been shown to be modulated by K concentration (Eder et al, 1996), though this effect appears to be restricted to very early in development (Klee et al, 1997).
388 In addition, IP3 gated ion channel; found in the autodendritic membrane
389 In an immunocytochemical study in zebrafish 60-70% of cells showed KA receptor mediated labelling
390 In an immunocytochemical study in zebrafish 60-70% of cells showed KA receptor mediated labelling
391 In an immunocytochemical study in zebrafish all cells resulted in NMDA receptor mediated labelling
392 In cell-attached patch-clamp recordings from the soma in guinea pig hippocampal slices, L-currents were found in 34% of the patches and found to have single channel conductances of 23-27 pS
393 In cell-attached patch-clamp recordings from the soma in guinea pig hippocampal slices, L-currents were found in 34% of the patches and found to have single channel conductances of 23-27 pS (Johnston et al. 1992;
394 In cell-attached patch-clamp recordings from the soma in guinea pig hippocampal slices, N-currents were found in 63% of the patches and found to have single channel conductances of 14 pS (Johnston et al. 1992;
395 In cell-attached patch-clamp recordings from the soma in guinea pig hippocampal slices, T-currents were found in 72% of the patches and found to have single channel conductances of 8 pS
396 In cell-attached patch-clamp recordings from the soma in guinea pig hippocampal slices, T-currents were found in 72% of the patches and found to have single channel conductances of 8 pS (Johnston et al. 1992,
397 In cilia; K 0.5 for Ca activation is 5 uM; most of Ca activated current is carried by chloride and persists in the absence of Na and K; Cl channel inhibitor 3',5-dichlorodiphenylamine-2-carboxylate (300uM) reduces current 90%; other Cl-channel inhibitors were tested [SITS, DIDS, A9C, DPC, NPPB, DCDPC]
398 In contrast, a study using radioactive in situ hybridization histochemistry looked at mRNA coding an NMDA glutamate binding protein and at NMDAR1 (an NMDAR subunit) expression and found heavy labeling for both in the pyramidal and polymorphic layers but little in the molecular layer
399 In gold fish retinal bipolar cells, four currents are observed: Ca currents, voltage- and calcium-dependent K currents, and Ih current
400 In mouse retinal bipolar cells, T-type Ca currents were recorded in soma, while L-type currents were recorded from axonal terminal
401 In mouse retinal bipolar cells, T-type Ca currents were recorded in soma, while L-type currents were recorded from axonal terminal
402 In patch recordings, "HVA-l channels reminiscent of L-type channels were occasionally encountered primarily in the more proximal dendrites" (and in the soma)
403 In PLTS cells “influx of Ca2+, while persistent depolarizations were due to influx of Na+. ”
404 In primary culture, GABA and glycine exert inhibitory actions on olfactory bulb neurons, mitral/tufted cells, granule and periglomerular cells
405 In retinal bipolar cells of bullfrog, both axon terminals and dendrites showed high GABA sensitivity mediated by both GABA(A) and GABA(C) receptors. GABA(A) and GABA(C) receptors may play different roles in the outer and inner retina and the differential complements of the two receptors on OFF and ON BCs may be closely related to physiological functions of these cells
406 In Salamander
407 In situ hybridization of three cloned SK channel subunits (SK1-3), the prime candidates likely to underlie Ca(2+)-dependent AHPs showed high levels of expression in regions presenting prominent AHP currents including CA1-3 regions of the hippocampus (SK1 and SK2), reticularis thalami (SK1 and SK2), supraoptic nucleus (SK3), and inferior olivary nucleus (SK2 and SK3)
408 In situ hybridization of three cloned SK channel subunits (SK1-3), the prime candidates likely to underlie Ca(2+)-dependent AHPs showed high levels of expression in regions presenting prominent AHP currents including CA1-3 regions of the hippocampus (SK1 and SK2), reticularis thalami (SK1 and SK2), supraoptic nucleus (SK3), and inferior olivary nucleus (SK2 and SK3)
409 In slices of rat brain at various postnatal ages was found that decay times of evoked IPSCs and spontaneous miniature IPSCs undergo progressive shortening during the first postnatal month
410 In slices that preserve mossy-fiber to granule cell synapses, Ach induced diverse responses in granule cells, one response being somatic current (nAChR also mediated postsynaptic currents, PSCs, which, however, were glutamatergic in nature, indicating a presynaptic mechanism. )
411 in SOBIV 297.
412 In the dorsolateral striatum, only parvalbumin mRNA-positive neurons expressed the mRNA encoding the potassium channel Kv3.1, a member of the Shaw family of potassium channels with rapid activation and inactivation kinetics, usually found in fast-firing neurons such as the basket cells of the hippocampus.”
413 In the hair-cell microvilli
414 In the hair-cell microvilli (Hudspeth AJ, Corey DP, others)
415 In triads made up of (i) a cholinergic axon, (ii) one or several periglomerular or granule cell dendrites, and (iii) usually one relay cell dendrite, asymmetric cholinergic synapses were selectively focused on dendrites (gemmules and spines) of periglomerular or granule cells.
416 In vitro, however, blocade of AMPA, NMDA, GABAA,D1 , D2, muscarinic receptors affect little the firing frequencies and patterns of cholinergic interneurons, indicating that these neurons are endogenously active and generate action potentials in the absence of any synaptic input
417 In vivo, the excitatory influence of STN contributes to the tonic discharge of SNr cells as shown by the marked reduction in SNr firing rate induced by a pharmacological blockade of STN activity
418 Inactivation of dendritic Na channel contributes to the attenuation of activity-dependent backpropagation of APs
419 Increased conductance may follow Ca impulses
420 Increased conductance may follow Ca impulses (Llinas and Walton 1998).
421 indicating that Ia synapses are distributed widely over soma-dendrites (confirmed by HRP labelling of Ia afferents on labelled motoneurones: reviewed in
422 Indirect evidence for this current was found in O-A interneurons
423 Indirect experimental evidence for dendritic Na channels was suggested by laminar filed potential studies
424 Individual branches can function as single integrative compartments where the fast oblique spike contains contributions from NMDA, VGCCs, and the A current
425 inferred
426 Inferred in
427 Inhibition of deep neurons (pyramidal and multipolar) by (presumed?) deep layer interneurons involves a fast Chloride and a slow potassium-mediated IPSP
428 Inhibitory interneurons, recorded mostly in the deeper part of layer II of piriform cortex, mediate fast IPSPs in principal cells and are activated at least partly through the axon collaterals of the principal cells
429 Input from dopaminergic neurons in the substantia nigra; causes small depolarization? sometimes a decrease in firing rate; modulates anomalous rectification of dendritic membrane (I IR)?
430 Intracellular recording from CA3 pyramidal neurons in a slice culture from rat found a slow excitatory response to Glu application in the presence of blocking agents for the ionotropic GluRs. Further experimentation revealed that ACPD could evoke the same response, which was due to the depression of I(K, Ca) and voltage-gated I(K)
431 Intracellular recording from CA3 pyramidal neurons in a slice culture from rat found a slow excitatory response to Glu application in the presence of blocking agents for the ionotropic GluRs. Further experimentation revealed that ACPD could evoke the same response, which was due to the depression of I(K,Ca) and voltage-gated I(K)
432 Intracellular recording from organotypic rat hippocampal cultures have shown that approximately 25% of single spikes in CA3 pyramidal neurons are followed by IPSPs at a fixed latency, presumeably a result of feedback inhibition from inhibitory interneurons. The addition of bicuculline (a competitive GABA(A) antagonist) completely abolished these responses, but they were insensitive to CGP35348, a GABA(B) antagonist
433 Intracellular recordings from sensorimotor cortex suggested that what activate IKCa persistently would not be calcium but some biochemical modification triggered by NMDA receptor activation
434 Intracellular recordings showed that Apamin-sensitive IKCa regulate pacemaker activity in these neurons
435 Intracellular recordings suggested different functional consequences for modulation of Ca2+ current subtypes. Based on the effects of specific organic Ca2+ channel blockers the sAHP was found to be coupled to N-, P-, and Q-type currents. P-type currents were coupled to the mAHP
436 Intracellular recordings: activation by I AHP causes unstable depolarizing plateau potentials; activated and modulated by 5-HT for decending raphe axons
437 Intracellular recordings: afterhyperpolarization potential inverses during repetitive impulse firing, limiting durations and frequency range of impulse firing
438 Intracellular recordings: AP5 blocks late component of EPSP elicited by olfactory nerve volley
439 Intracellular recordings: AP5 blocks late component of EPSP response to olfactory nerve volley
440 Intracellular recordings: AP5 blocks late component of EPSP response to olfactory nerve. volley
441 Intracellular recordings: AP5 blocks late component of EPSP response to olfactory nerve. volley
442 Intracellular recordings: CMQX and NBQX applied at the soma completely block short duration (i.e. near soma) single fiber EPSPs
443 Intracellular recordings: CNQX blocks early component of EPSP elicited by olfactory nerve volley
444 Intracellular recordings: CNQX blocks early component of EPSP elicited by olfactory nerve volley nerve volley
445 Intracellular recordings: CNQX blocks early component of EPSP response to olfactory nerve volley
446 Intracellular recordings: IPSP blocked by bicuculline and low Cl-
447 Intradendritic recordings show Ca-dependent plateau potentials and Ca impulses
448 Intrastriatal stimulation-induced release of ACh from presynaptic nerves hyperpolarizes cholinergic interneurons by activating muscarinic receptors (probably M2) located on somatodendritic region
449 Involvement of presynaptic NMDA receptors in cerebellar long-term depression at parallel fiber-Purkinje cell synapses
450 Ionophoretic glutamate applied to dendrites depolarizes Purkinje cells. Glu is released from parallel fibers of granule cells
451 IP3 gated ion channel; found in soma by
452 IPSP blocked by bicuculline
453 IPSP blocked by bicuculline and low Cl-
454 IPSPs elicited by monoamines in pyramidal cells result from a convergence of inputs from populations of layer II/III interneurons that are activated by one, two or all three of the following monoamines 5-HT, NE, and DA.
455 Isolated rod-dominant on-center bipolar cells respond to GABA, the highest sensitivity of which being located at the axon terminal
456 It contributes to the spontaneous activity of these cells and to the tonic inhibition of CA1 pyramidal neurons in the hippocampus
457 It has also been found that CNQX does not block the intracellular calcium concentration increase normally associated with stratum lucidum stimulation
458 It has also been found that CNQX does not block the intracellular calcium concentration increase normally associated with stratum lucidum stimulation
459 It has also been shown (using whole and perforated patch recording from acutely isolated CA3 pyramidal neurons) that application of Glu and quisqualatic acid (in the presence of D-AP5, an NMDAR-antagonist, and CNQX, an AMPAR antagonist) results in responses that consist of an inward current that may be preceded by an outward current. Both of these currents are affected by bath [K] and they had different pharmacological properties (Harata et al, 1996).
460 It has also been shown (using whole cell and perforated patch recording from acutely isolated CA3 pyramidal neurons) that application of Glu and quisqualatic acid (in the presence of D-AP5, an NMDAR-antagonist, and CNQX, an AMPAR antagonist) results in responses that consist of an inward current that may be preceded by an outward current. Both of these currents are affected by bath [K] and they had different pharmacological properties (Harata et al. 1996 #8680866).
461 It has been shown that activation of these receptors could facilitate transmitter release. Their activation is very fast (<10 ms) and lasts for seconds, and could contribute to the short-term plasticity characteristics of mossy fiber synapses
462 it has been shown to occur at mossy fiber synapses even in the presence of NMDA receptor antagonists under certain conditions
463 It has been suggested in rats that GABA(B) receptors modulate dendrodendritic inhibition primarily by inhibiting granule cell calcium channels and reducing the release of GABA
464 It has been suggested that the pharmacologically separable components of the HVA current in these neurons do not differ significantly in kinetics
465 It has been suggested that this current is not involved in the generation of AHP but (with other HVA currents) contributes to the inward currents that regulate interspike intervals during repetitive firing
466 It has been suggested that voltage-gated calcium channels play a role in LTP
467 It has been suggested that voltage-gated calcium channels play a role in LTP (Johnston et al. 1992), and it has been shown that nimodipine (an L-channel antagonist) prevents certain mossy fiber LTP-types from taking place
468 It was decreased by cannabinoids
469 It was shown that stimulation of PG cells results in self-inhibition: release of GABA from an individual PG cell activates GABA(A) receptors on the same neuron
470 It was was blocked by linopirdine in a reversible, concentration-dependent manner
471 Kinetic properties were studied using the whole-cell patch-clamp technique
472 Kinetic, pharmacological, and structural properties of these receptors were studied using patch-clamp techniques and single-cell reverse transcriptase polymerase chain reaction
473 Korf et al, 1976; Cheramy et al 1981) by backpropagating impulse
474 L-type ICa was found only in cells that retained axon terminals ramifying in the inner plexiform layer
475 Labeling for glutamic acid decarboxylase (GAD), the enzyme that synthesizes GABA, is heavy in the molecular layer of CA1
476 Large EPSPs activate I IR, increasing the membrane resistance, shortening the dendrites electrotonically, making the cell more sensitive to subsequent inputs (see
477 Lateral circuits contribute to the inhibitory surround. The bipolar neurons release glycine or GABA onto presynaptic bipolar neurons and ganglion cell dendrites
478 Layer 2/3 fast-spiking interneurons (most of which are basket cells) received the strongest excitatory input (presumably glutamatergic) from layer 4
479 Layer 4 basket cells in cat visual cortex receive asymmetric synapses from layer 6 pyramidal (~43%), the spiny stellate (44%) and thalamic afferents (13%)
480 Layer 4 basket cells in cat visual cortex receive excitatory input from neighboring spiny neurons, resulting in large excitatory EPSPs. One third of spiny cell-smooth cell pair were connected reciprocally (postsynaptic targets include local spiny stellate, pyramidal cells, as well as smooth neurons), but the postsynaptic IPSPs evoked by basket cells are slower, GABAergic, probably of GABAA type
481 Layer Ia horizontal cells receive a very small number of symmetrical synapses (presumably GABAergic?), in contrast to interneurons of the deeper layers of the piriform cortex -- globular, multipolar cells
482 Layer-4 basket cell axons make lateral connection isotropically near cell body ( 50 microm radius), but beyond this core region, anisotropically, preferably within a particular angular sectors cell body
483 Leads to a fast EPSP which allows an influx of cations. This can work with the M1 receptors to switch the cell from burst to tonic mode
484 lighter staining for GABA/GAD; SOBiv p132). Cartwheel cells produce IPSPs in pyramidal cells (see
485 Llinas and Walton 1990).
486 low density
487 Low threshold calcium spikes were antagonized by T-channel blockers in rat
488 Low threshold inactivating Ca2+ current
489 Low-voltage-activated (LVA) and high-voltage-activated (HVA) Ca2+ currents were observed in the isolated rod bipolar cell terminal recordings
490 Macropatch clamp and intracellular recordings in guinea pigs suggested that the pattern of Ca2+ spike firing in the dendrites of Purkinje cells is dynamically modulated by a highly aminopyridine-sensitive K+ current, and probably also by a Ca2+-activated potassium current
491 Mammal. (See SOBiv p140).
492 Many amacrine-to-ganglion cell synapses accumulate glycine
493 Many authors have described the activation of dendritic voltage activated Ca channels
494 Matsui K, Hosoi N and Tachibana M, 1998
495 May generate long delays contributing to temporal patterns (Ketchum and Haberly 1991); may play a role in epileptogenesis
496 Mechanisms underlying suppression of this current by odorants were investigated in newt ORNs using the whole-cell version of the patch-clamp technique
497 Membrane patches recorded in the cell-attached patch configuration from the soma and apical dendrites revealed an Ih that increased over sixfold from soma to distal dendrites. Ih demonstrated a mixed Na+-K+ conductance and was sensitive to low concentrations of external CsCl. As a result of Ih the propagation of subthreshold voltage transients is directionally specific.The elevated dendritic Ih density decreases EPSP amplitude and duration and reduces the time window over which temporal summation takes place
498 mGluR2 knockout mice show normal LTP and synaptic transmission but not LTD
499 Microionophoretic studies
500 Mitral-cell soma-dendrites act as a presynaptic terminal to the granule cell; the circuit is recurrent onto the injected cell; and the inhibitory transmitter is GABA
501 MK801 (an NMDAR antagonist) blocks the transient intracellular Ca2+ release normally associated with stratum lucidum stimulation (found by simultaneous Ca imaging and intracellular recording in rat brain slices by
502 Modulation of synaptic transmission between granule cells and Purkinje cells via presynaptic GABAB receptors
503 Modulation of this current by dopamine was studied using standard patch-clamp techniques.
504 Morphological evidence of local contact by pyramidal neurons
505 Mose retinal ganglion
506 Most layer 2/3 pyramidal neurons and interneurons received inhibitory input (presumably GABAergic) from neighboring interneurons in layer 2/3
507 Mouse
508 mRNA of A-channel subunit Kv4.2 is expressed predominantly in granule cells. (In contrast, that of Kv4.3, also of A-channel, is expressed predominantly in periglomerular cells)
509 mRNA of A-channel subunit Kv4.2 is expressed predominantly in granule cells. (In contrast, that of Kv4.3, also of A-channel, is expressed predominantly in periglomerular cells)
510 mRNA of A-channel subunit Kv4.3 is expressed predominantly in periglomerular cells. (In contrast, that of Kv4.2, also of A-channel, is expressed predominantly in granule cells)
511 N-type Ca2+ currents in rat neostriatal cholinergic interneurons is reduced through D2 receptor activity
512 Na action potentials support backpropagating impulses
513 Na impulses may underly "fast prepotentials" that boost distal EPSPs
514 NaV1.1 is present in the soma and proximal dendrites, NaV1.6 is robustly present in cell bodies and dendrites, and NaV1.7 is absent from the cell
515 NaV1.2 is substantially present throughout the dendrites, NaV1.1 is present in the soma and proximal dendrites, NaV1.6 is robustly present in cell bodies and dendrites, and NaV1.7 is absent from the cell
516 Neostriatal cholinergic interneurons fire irregularly but tonically in vivo. The summation of relatively few depolarizing potentials and their temporal sequence are thought to underlie spike triggering and the irregularity of action potential timing, respectively
517 Nitric oxide, released from both mitral and granule cells, is involved in olfactory memories and may act as a retrograde and/or intracellular messenger. However, only mitral cells expressed guanylyl cyclase subunits.
518 NMDA and AMPA conductances properties were studied using patch-clamp recordings in morphologically identified cells in slices prepared from surgically removed medial temporal lobe specimens of epileptic patients (14 specimens from 14 patients
519 NMDA and AMPA conductances properties were studied using patch-clamp recordings in morphologically identified cells in slices prepared from surgically removed medial temporal lobe specimens of epileptic patients (14 specimens from 14 patients). The wide range of changes in the slope conductance of the NMDA EPSCs suggests that the NMDA-receptor-mediated conductance could be altered in human epileptic DGCs
520 NMDA iontophoretically applied to basal dendrites evoked inward currents near resting potential. Changing levels of bath calcium concentration downwards by 50% caused an increase in the inward current
521 NMDA receptor is required for DDI (dendrodendritic inhibition) since IPSC was completely blocked by AP-5. Ineffectiveness of AMPA receptor-mediated EPSPs to activate the granule cells may be due to their intrinsic membrane properties.
522 NMDA receptors play a critical role in dendrodendritic inhibition between mitral and granule cells. Moreover, N- and P/Q type calcium channels are involved.
523 NMDA reversibly depresses postsynaptic currents, through a trans-synaptic mechanism that involves release from parallel fibers nitric oxide that decreases the glutamate sensitivity of the Purkinje cell
524 Nomarski optics and infrared videomicroscopy were used to demonstrate the existence of a TTX-sensitive persistent Na+ conductance (INaP) in identified medium-sized neostriatal neurons
525 Nucleated patches revealed a fast component highly sensitive to external 4-AP and TEA (~57% of total K+ current) and a slow component that was sensitive to high concentrations of TEA, but insensitive to 4-AP (~25% of total K+ current)
526 Numerous authors (e.g.,
527 ON beta Ganglion cells. ON beta Ganglion cells respond to ionophoresed GLU and GLU agonists, and are blocked by GLU antagonists (SOBiv p238). Ganglion cells express GLUR and NMDAR
528 on spines (SOBiv p126,130). The neurotransmitter is GLU
529 One STN regulator is the serotonin (5-HT) system. The STN receives a dense 5-HT innervation. 5-HT1A, 5-HT1B, 5-HT2C, and 5-HT4 receptors are expressed in the STN. 5-HT may regulate the STN via several mechanisms."
530 Original intracellular recordings in vivo
531 P)
532 P2
533 p395).
534 p396
535 p396).
536 p396.
537 p397).
538 p397.
539 Paired recordings in slices showed excitatory transmission mediated solely by transmitter spillover between mitral cells. Dendritic glutamate release causes self-excitation via local activation of NMDA receptors, and generates NMDA receptor-mediated responses in neighbouring cells. It is suggested that this simultaneous activation of neighbouring cells by a diffuse action of glutamate provides a mechanism for synchronizing olfactory principal cells
540 Paired whole-cell recording revealed reciprocal excitatory connections between mitral cells. Pharmacological analysis suggested that it could be mediated by both AMPA and NMDA receptors
541 Patch Clamp recordings revealed density levels are similar to that found in the soma, with slightly different kinetics
542 Patch recordings
543 Patch recordings indicate channels similar in basic characteristics to one or more of the HVAm channel types (most likely Q- or R-type channels)
544 Patch recordings of back propagating impulses in dendrites. Variable densities of active channels support variable extents of backpropagating impulse in the dendrites
545 Patch recordings yield an approximate channel density of 28 pS/micron^2 in juvenile rats < 4 wks of age, rising to 61 pS/micron^2 in older rats. Channel density was similar in other dendritic compartments
546 Patch recordings yield an approximate channel density of 45 pS/micron^2 (compared with 28 pS/micron^2 in dendrites) in juvenile rats < 4 wks of age, rising modestly to 56 pS/micron^2 (compared with 61 pS/micron^2 in dendrites) in older rats
547 Patch recordings yield an approximate channel density of 7 pS/micron^2 in juvenile rats < 4 wks of age, rising to 10 pS/micron^2 in older rats. Ca channel density was similar in other dendritic compartments, and in general lower than Na channel density
548 Patch recordings yield an approximate channel density of 7 pS/micron^2 in juvenile rats < 4 wks of age, rising to 10 pS/micron^2 in older rats. Ca channel density was similar in other dendritic compartments, and in general lower than Na channel density
549 Patch-clamp recordings from human cells showed N-type, L-type and T-type currents that had similar pharmacological and kinetic characteristics as in control rats. The current density was significantly larger in human and in the kainate model compared to cells isolated from adult control rats
550 Patch-clamp recordings reveal a high density of A-type K channels in the dendritic tree, which increases with distance from the soma
551 Patch-clamp recordings reveal A-type K channels in the soma
552 Patch-pipette recordings found no evidence for a ?sag? in hyperpolarizing responses, suggesting that this current is not present in these neurons
553 Perforated whole-cell voltage-clamp recordings showed that dopamine modulates the L-type Ca2+ channels in rat olfactory receptor neurons via a voltage-independent mechanism
554 Perhaps the principal function of these neurons is to release SOM, NOS, and/or NPY, all of which could exert slower neuromodulatory effects on their postsynaptic targets rather than fast synaptic effects. For example, SOM has been shown to exert a potent presynaptic inhibition on GABA release at SPN–SPN synapses.”
555 Perhaps the principal function of these neurons is to release SOM, NOS, and/or NPY, all of which could exert slower neuromodulatory effects on their postsynaptic targets rather than fast synaptic effects. For example, SOM has been shown to exert a potent presynaptic inhibition on GABA release at SPN–SPN synapses.”
556 Periglomerular cells respond to microapplication of GABA, acetylcholine, norepinephrine and glycine with the activation of distinct ionic currents.
557 PG cells closely resembled previously described periglomerular cells in their morphology. During current clamp recording these neurons were characterized by their lack of action potentials upon depolarization. Consistent with these results no Na+ currents could be elicited in voltage clamp experiments. Two types of outward K+ currents were distinguished: one which inactivated and one which did not.
558 PKC may have a negative feedback role in modulating excitation by 5-HT in piriform cortical interneurons
559 PLTS cells exhibited unique firing properties due to Ca*+-dependent low-threshold spikes and Na+-dependent persistent depolarized spikes, in addition to Na+-dependent fast spikes.”
560 PLTS interneurons receive numerous synaptic contacts on their proximal dendrites from both cholinergic and dopaminergic axons, as well as onto their distal dendrites, which receive asymmetric synaptic inputs from the cortex.”
561 PLTS interneurons receive numerous synaptic contacts on their proximal dendrites from both cholinergic and dopaminergic axons, as well as onto their distal dendrites, which receive asymmetric synaptic inputs from the cortex.”
562 PLTS interneurons were found to evoke only sparse and relatively weak GABAergic IPSCs in SPNs.”
563 Possible
564 Potassium-induced glutamate release from granule cells is dependent on the entry of Ca++ through multiple types of Ca-channel including N-, L-, P/Q-types; a number of these channel subtypes seems to be involved in the presynaptic modulation, by GABAB receptors, of potassium-induced glutamate release
565 Potentiation of intrinsic excitability was induced by relatively weaker inputs than those that induce potentiation of synaptic efficacy; NMDA receptors are involved in both aspects of potentiation
566 pp385,389,393-395,407).
567 Presence of Kv4.2 but not Kv1.4 subunits in the somatodendritic membrane. Depolarization-activated potassium currents in cholinergic interneurons were dominated by a rapidly inactivating, K+-selective A current that became active at subthreshold potentials.
568 Presence of Kv4.2 but not Kv1.4 subunits in the somatodendritic membrane. Depolarization-activated potassium currents in cholinergic interneurons were dominated by a rapidly inactivating, K+-selective A current that became active at subthreshold potentials
569 Presence of Kv4.2 but not Kv1.4 subunits in the somatodendritic membrane. Depolarization-activated potassium currents in cholinergic interneurons were dominated by a rapidly inactivating, K+-selective A current that became active at subthreshold potentials
570 Presence of Subthreshold-operating transient (A-type) K(+) currents (I(SA)s), as indicated by an accesspry subunit that accelerates the kinetics of this current
571 Present in lower density than in the cilia
572 Present in lower density than in the cilia.Properties of this channel in rat, and its functional interplay with the CNG channel, were studied by using inside-out membrane patches excised from ORN dendritic knobs/cilia
573 presumably GABA inhibition (summarized in Young and Oertel,
574 presumed
575 Presynaptic terminal and axon NMDAR's have been found withimmunocytochemical techniques
576 Probably.
577 Prolongation of ISI through a D1 dopamine receptor-mediated enhancement of the afterhyperpolarization (AHP)
578 Properties of K+ outward currents were investigated in human DG cells from 11 specimens obtained from patients with temporal lobe epilepsy. An IK was observed in all cells. The average current density, the time-dependent decay, and the resting membrane characteristics were not significantly different between patients with and without Ammon Horn Sclerosis. The V1/2(inact) was shifted in a hyperpolarizing direction in AHS (-67.7mV) compared with that in hippocampi not showing AHS (-47.7mV)
579 Properties of potassium outward currents were investigated from 11 specimens obtained from patients with temporal lobe epilepsy. An IK but not IA or inwardly rectifying potassium currents, were observed in all cells
580 Properties of this channel in rat, and its functional interplay with the CNG channel, were studied by using inside-out membrane patches excised from ORN dendritic knobs/cilia
581 Properties of this current and its modulation by PKA were studied using whole-cell patch-clamp recording techniques
582 provide evidence that activation of these receptors is necessary for LTP induction
583 provide evidence that activation of these receptors is necessary for LTP induction .
584 Quantitative autoradiography has been used to localize [3H]AMPA binding sites. In CA3, labeling was substantially heavier in s. pyramidale than in s.radiatum and s. lacunosum-moleculare
585 Quantitative autoradiography has been used to localize [3H]AMPA binding sites. It was found that AMPARs are found in a high concentration in the hippocampus relative to other areas in the brain. In CA3, labeling was substantially heavier in s. pyramidale than in s.radiatum and s. lacunosum-moleculare
586 Quantitative autoradiography has been used to localize sites at which L-[3H]-glutamate is displaced by NMDA. The labelling of these receptors was somewhat lower than in CA1 overall, being highest in s. oriens and s. radiatum and very low in s.pyramidale and s. lucidum
587 quote from the review in Llinas and Walton 1990).
588 Rat
589 Re: PG cells: Two types of outward K+ currents were distinguished: one which inactivated and one which did not.
590 Recording from dissociated neurons using intracellular and whole-cell voltage-clamp recordings showed that carbachol can act at M1-like muscarinic receptors to reduce the membrane K+ conductances and excite the neostriatal neurons
591 Recordings from acute brain slices and in anesthetized rats using whole-cell recordings and Ca2+ imaging found that backpropagation of action potentials into the dendritic arbor is actively supported by Na+ channels both in vitro and in vivo.
592 Recordings from acute brain slices and in anesthetized rats using whole-cell recordings and Ca2+ imaging found that single action potentials evoke little or none Ca2+ influx in the dendritic tuft, unless is paired with synaptic input
593 Recordings from acute brain slices and in anesthetized rats using whole-cell recordings and Ca2+ imaging found that single action potentials evoke substantial Ca2+ influx in the apical trunk.
594 Recordings from membrane patches of dendrites and soma reveal fast and slow responses to fast application of glutamate, mediated by AMPA amd NMDA receptors, respectively
595 Recordings from membrane patches of dendrites and soma reveal fast and slow responses to fast application of glutamate, mediated by AMPA and NMDA receptors, respectively
596 Recordings in slices showed that D1 receptor activation can either inhibit or enhance evoked activity, depending on the level of membrane depolarization, by modulating an L-type Ca2+ conductance
597 Recordings in slices showed that GABA inhibition was mediated by GABA(B) receptors in the dendrites and GABA(A) receptors in the soma and dendrites
598 Recordings using infrared-guided laser stimulation combined with whole cell recordings revealed a highly nonuniform distribution. Hot spots, with amplitude and integral of glutamate-evoked responses three times larger than responses evoked at neighboring sites, were detected. It appeared that the larger responses evoked resulted from an increase in activation of both AMPA and NMDA receptors. There was no correlation with branch points
599 Recordings using the intracellular perfusion method showed no differences between the I-V characteristics of CA1 and CA3 neurones for this current. In contrast to this, the steady-state inactivation of both types of neurones was significantly different
600 report the presence and function of Ih.
601 Response of isolated bipolar cells to glycine
602 Response to glutamate in isolated bipolar cells
603 Reversed chloride gradients, demonstrated by cytochemical methods, may be responsible for excitatory GABA effects on selected periglomerular neurons
604 reviewed by
605 Reviewed in
606 reviewed in
607 Reviewed in
608 reviewed in
609 reviewed in
610 Reviewed in
611 Reviewed in
612 Reviewed in
613 reviewed in Haberly 1998).
614 reviewed in Llinas and Walton, 1990).
615 reviewed in McCormick 1998).
616 reviewed in Shepherd 1998). Variable densities of active channels support variable extents of backpropagating impulse in the dendrites
617 Rhodopsin (rods) and red, green and blue opsins (cones), in disc membranes of the distal segment.
618 Rhodopsin (rods) in disc membranes of the distal segment.
619 see also
620 see also
621 see also
622 see also
623 see also Felix and MacLennan, 1971).
624 see also Tseng and Haberly 1989b; reviewed in
625 see Burke 1998 for references). Single-fiber Ia EPSPs have widely varying shapes
626 See SOBiv p140).
627 Selective localization of GABA receptors at symmetric synapses ( and of gluR at asymmetric synapses.)
628 Sensitive to TTX. This generates the impulses that propagate into the axon
629 Sensitive to TTX. This plateau potential underlies impulse bursting
630 Serotonin produced a slowly developing and long-lasting suppression of IM leading to depolarization end excitation
631 Sherman and Koch, 1990).Using electrophysiological recordings and imaging, the density of these channels was found to rapidly decrease with distance from soma and clustered in high density around the base of dendrites
632 showed that the proximal dendrites and somata of hippocampal neurons label for L-type Ca2+ channels and that these channels tend to cluster near the bases of the neural processes. In patch recordings, "HVA-l channels reminiscent of L-type channels were occasionally encountered primarily in the more proximal dendrites" (and in the soma)
633 Silent synapses during development
634 Simultaneous recordings were carried out in visual cortical slices. Assuming open probability of non-NMDA receptor channels to be 0.7, it is suggested that the number of channels available for synaptic transmission between individual pyramidal cells would be 74 (kittens) and 59 (rats)
635 Simultaneous whole-cell recordings, made from the soma and dendrites rat brain slices, showed that AP evoked by either current pulses or synaptic stimulation of parallel or climbing fibers, always occurred first at the soma and decreased in amplitude with increasing distance into the dendrites. Simultaneous somatic and axonal recordings showed that these action potentials were initiated in the axon
636 Simultaneous whole-cell recordings, made from the soma and dendrites rat brain slices, showed that AP evoked by either current pulses or synaptic stimulation of parallel or climbing fibers, always occurred first at the soma and decreased in amplitude with increasing distance into the dendrites. Simultaneous somatic and axonal recordings showed that these action potentials were initiated in the axon. Outside-out patches excised from the soma and dendrites up to about 100um revealed a channel density decreasing with distance from the soma.
637 Single action potential backpropagations show dichotomy of either strong attenuation (26-42%) or weak attenuation (71-87%). The dichotomy seems to be conferred primarily by differences in distribution, density, etc. of voltage dependent sodium and potassium channel (A-type, especially ) along the somatodendritic axis
638 single fiber EPSPs:
639 Single unit extracellular recordings showed a short latency GABAA inhibition that arises from the axon collaterals of pars reticulata projection neurons
640 Single-cell-reverse transcription-polymerase chain reaction analysis of glycine receptor-subunit expression was combined with whole-cell recordings from acutely isolated cholinergic interneurons. Subunits alpha2, beta, alpha3, were found to be associated with receptor properties such as efficacy and desensiutization. Celllular localization of receptors unclear, but presumably on soma (?)
641 Single-channel and whole-cell recording identified three types of current: a transient inward sodium current and a transient and a sustained outward potassium current
642 Single-channel recordings from inside-out membrane patches excised from toad chemosensory cilia showed the presence of 4 different types of KCa channels, with unitary conductances of 210, 60, 12, and 29 and 60 pS, high K+-selectivity, and Ca2+ sensitivities in the low micromolar range
643 Single-fiber Ia EPSPs have widely varying shapes
644 Slow inactivation of sodium channels in dendrites and soma will modulate neuronal excitability in a way that depends in a complicated manner on the resting potential and previous history of action potential firing
645 Slow second messeger pathway that leads to a reduction in K+ current. This can switch the cell from burst to tonic mode
646 SNr GABA neurons express a strong Kv3-like current with fast activation and slow inactivation kinetics that is required for the sustained high frequency firing capability in these neurons"
647 SNr neurons contain both muscarinic
648 sobiv 242). This is excitatory
649 sobiv 242). Dendritic compartments not specified.
650 SOBiv p128). Granule cells are similar to cerebellar granule cells (SOBiv p132).
651 SOBiv p131).
652 SOBiv p140). Such sequences are seen after acoustic stimulus
653 SOBiv p140).(P1)
654 sobiv p217)
655 sobiv p217), boosting ganglion cell transients, increasing sensitivity to motion
656 sobiv p217). These nicotinic receptors desensitize rapidly
657 SOBiv p238). Multiple subunits of GLUR and NMDAR are present
658 SOBiv p238). Some bipolar cells contain glycine
659 SOBiv p238).Clusters of glycine receptors were found on the somatodendritic membranes of Alpha ganglion cells
660 SOBiv p243).
661 SOBIV p316
662 SOBIV p316).A study indicates that synaptic activation of these receptors increases inhibitory activity in relay neurons by increasing output of presynaptic dendrites
663 SOBIV p317).
664 SOBiv p88). Glutamate is released from Ia terminals
665 SOBiv p91.
666 SOBiv p94). Glycine ionophoresis mimics Ia IPSPs (reviewed by
667 SOBiv p94). Ia IPSPs are blocked by strychnine, a known blocker of Glycine receptors (SOBiv p94).
668 SOBiv p95.
669 SOBiv p96).
670 Soma and proximal apical dendrites receive mainly flattened (FL) or pleiomorphic (PL) vesicle synapses on their trunks. These are correlated with IPSPs (SOBiv p128,130-1). Cartwheel cells stain for CLY
671 Somatic and Dendritic patch recordings showed an even density of Na channels (120pSum-2) up to 350 um from the soma along the primary dendrite to theorigin of the glomerular tuft
672 Some diferences in the neurons in the deeper layers (v.s. those in the superficial layers) can be accounted for by differences in the IA channel in the cells
673 Some kinetic properties of this current were studied in cell-attached recordings in rats
674 Spike-triggered calcium entry shaped the falling phase of the action potential waveform and activated calcium-dependent potassium channels
675 Spontaneous and electrically driven GABAergic synaptic inputs to PG cells come possibly from other interneurons in the glomerular layer.
676 Spontaneous firing was driven by the combined action of a sodium current and the hyperpolarization-activated cation current (I(h)), which together ensured that there was no zero current point in the subthreshold voltage range. Spike-triggered calcium entry shaped the falling phase of the action potential waveform and activated calcium-dependent potassium channels
677 spontaneously released dopamine from dopamine dendrites induces tonic activation of D1-like receptors and exerts a tonic excitatory influence on SNr GABA neurons"
678 spontaneously released dopamine from dopamine dendrites induces tonic activation of D1-like receptors and exerts a tonic excitatory influence on SNr GABA neurons."
679 Starburst amacrine cells release a pulse of Ach onto ganglion cells dendrites
680 Steady-state inactivation curve is 10 mV more depolarized in SP cells in endopiriform nucleus. "Modelling analysis suggested that this difference is sufficient to explain the more depolarized membrane potential of deep cells, and results in a 2-fold decrease in latancy of the first spike evoked by depolarizing steps"
681 STN neurons containing a4ß2 nAChRs (a4ß2 neurons) received more glutamatergic inputs, and preferentially innervated GABAergic neurons in the substantia nigra pars reticulata. In contrast, STN neurons containing a7 nAChRs (a7 neurons) received more GABAergic inputs, and preferentially innervated dopaminergic neurons in the substantia nigra pars compacta."
682 Striatal FSIs make [GABAergic] synapses onto both direct and indirect path- way SPN. The biophysical properties of the synaptic contacts do not differ and exhibit short-term depression. Further, single FSI often make synapses with both types of SPN”
683 Strychnine-sensitive glycine receptors are present on a subpopulation of the cholinergic interneurons in rat caudatoputamen, supporting the hypothesis that (excitatory) glycine receptors inducing striatal release of [(3)H]acetylcholine may be localized to cholinergic neurons
684 Substantial in most deep pyramidal and multipolar cells; generates hyperpolarizing potentials lasting several seconds; as I AHP contributes to rapid spike frequency adaptation; blocked by cholinergic agonists
685 Subthalamic nucleus neurons make glutamatergic connections on neurons of the globus pallidus.
686 Subthalamic nucleus neurons receive input from GABAergic globus pallidus neurons through GABA-A receptors.
687 Subthreshold membrane potential oscillations are blocked by bath application of tetrodotoxin (TTX), a potent Na(t)-current antagonist, in rats 3-17 days old
688 Suggested.
689 suggesting the presence of mGluRs.
690 suggesting the presence of mGluRs.
691 Synapse of type 2
692 Synaptic inhibition of mitral cells: Yamamoto et al, 1962;
693 T-type calcium current recorded in bipolar cells in slice in mouse
694 T-type channels are less dense in the soma than in the dendrites
695 The A current increases with distance from the soma normalizes Ca+ signals during AP propagation
696 The action potential has a pronounced Ca component on its falling phase
697 The amplitude of ensemble K+ currents in cell-attached patches decreased along the apical dendrite as the distance from the soma increased, with a slope of -0.9 +/- 0.3 pA per 100um. In nucleated outside-out patches from soma in acute slices of sensorimotor cortex from 13- to 15-day-old Wistar rats some patches contained only I-A-like channels, other contained only IK-like channels that did not inactivate or inactivated slowly, and the remainder contained mixtures of both types. The amount of IA and IK depended weakly on distance along the primary apical dendrite from the soma. The amplitude of IA increased, while the amplitude of IK decreased
698 the back-propagating action potential may be important for the dendritic release of dopamine"
699 The balance between synaptic (glutamatergic) and non-synaptic conductance indicates that the synapse will not shunt the cell and the conductance ratio serves to maximize incremental gain at the photoreceptor to ON bipolar synapse.
700 The basal conductance of unstimulated frog ORN was investigated using whole-cell and perforated-patch recording. It was found that under physiological conditions, gating of CNG channels contributes approximately 0.06 nS to the resting neuronal conductance
701 The baskets formed by inhibitory basket cells have high concentrations of glutamic acid decarboxylase (GAD), the enzyme that synthesizes GABA
702 The CA1 oblique dendrites (also called radial oblique) are the main target of the Schaffer collaterals from CA3, and are therefore the primary sites of generation of LTP.
703 The cellular localization of GABAB binding was investigated using lesion techniques. It was suggested that the majority of cerebellar molecular layer GABAB binding sites are located on Purkinje cell dendrites. During development binding in the molecular layer peaks between postnatal day 14 and postnatal day 28 and then decreases to adult levels
704 The contribution of a fast (IAt), and a slowly (IAs)-inactivating A-currents were studied in slices. The results suggest a role for these currents to define the limits on the depolarized state
705 The contribution of an inwardly rectifying current (IKir) were studied in slices. The results suggest that the hyperpolarized state is determined principally by this current
706 The developmental evolution of Ca-dependent spikes in the tuft was investigated using simultaneous somatic and dendritic recordings
707 The distribution of GABAA and GABAB receptors was studied with patch-clamp recording in combination with infrared-guided laser stimulation to release GABA photolytically. The data suggest that relatively more GABAA receptors are located at the apical dendrite and relatively more GABAB receptors near the soma
708 The distribution of the P-type calcium channel in the mammalian central nervous system has been demonstrated immunohistochemically by using a polyclonal specific antibody. Electron microscopic localization revealed labeled patches of plasma membrane on the soma, main dendrites, spiny branchlets, and spines; portions of the smooth endoplasmic reticulum were also labeled. Strong labeling was present in the periglomerular cells of the olfactory bulb, ...etc
709 The effects of glutamate on SNr cells is mediated by the three principal types of glutamate receptors: a-amino 3hydroxy-5methyl- 4-isoxaline propionic acid/kainate (AMPA), N-methyl-D aspartate (NMDA) and metabotropic receptors [mGluR1 and mGluR5]” Reviewed in
710 The effects of glutamate on SNr cells is mediated by the three principal types of glutamate receptors: a-amino 3hydroxy-5methyl- 4-isoxaline propionic acid/kainate (AMPA), N-methyl-D aspartate (NMDA) and metabotropic receptors” Reviewed in
711 The effects of intracellular calcium buffering on electrical tuning were studied in hair cells at apical and basal cochlear locations tuned to 100 and 300 Hz. Ca2+ imaging revealed about twice as many hotspots of Ca2+ entry during depolarization in high-frequency compared to low-frequency hair cells. It is suggested that each KCa channel is gated by Ca2+ entry through a few nearby Ca2+ channels, and that Ca2+ and KCa channels occupy, at constant channel density, a greater fraction of the membrane area in high-frequency cells than in low-frequency cells
712 The effects of intracellular calcium buffering on electrical tuning were studied in hair cells at apical and basal cochlear locations tuned to 100 and 300 Hz. High conductance KCa channels were 2-fold less Ca2+ sensitive in high-frequency than in low-frequency cells. It is suggested that each KCa channel is gated by Ca2+ entry through a few nearby Ca2+ channels, and that Ca2+ and KCa channels occupy, at constant channel density, a greater fraction of the membrane area in high-frequency cells than in low-frequency cells
713 The effects of this current on the firing properties were studied in brainstem slices
714 The fast and slow components of EPSCs were studied using whole cell patch clamp recordings
715 The functional properties of AMPA receptors were studied in acute slices. It was found that AMPARs expressed in different types of basal ganglia neurons were markedly diverse
716 The functional properties of NMDA receptors were studied in acute slices. Little variability in functional properties was found in different types of basal ganglia neurons
717 The GABABR1a antibody selectively marked the neuropil in layer Ia, where afferent olfactory fibers and intrinsic GABAergic axons terminate on the distal apical dendrites of pyramidal neurons. GABABR1a may be involved in feedforward synaptic circuits
718 The globus pallidus, a neuronal nucleus involved in the control of motor behavior, expresses high levels of histamine H3 receptors (H3Rs) most likely located on the synaptic afferents to the nucleus.”
719 The GP is mainly made up by two populations of GABAergic neurons, with the predominant one projecting to the subthalamic nucleus while a second group sends projections to the striatum."
720 The kinetic properties of this current have been studied in mice using voltage clamp with whole-cell patch recordings
721 The kinetic properties of this current were studied in cell-attached recordings in rats
722 The kinetic properties of this current were studied using the whole-cell voltage-clamp method in acutely isolated cells. No significant differences were found after induction of status epilepticus
723 The kinetics of GABA currents were studied using flash photolysis of caged GABA
724 The kinetics properties of this current were studied using whole-cell recording from dissociated neurons. Unlike other cells, recovery from inactivation was accompanied by a sizeable ionic current. It was suggested that the current flowing during this recovery may depolarize the cells immediately after an AP, promoting the typical high-frequency firing of these neurons (complex spike)
725 The main synaptic afferents to GP are striato-pallidal GABAergic axons."
726 The mGluRs belonging to group I and II are located on the axon terminals of striatal cholinergic interneurons, their activation resulting in facilitation and inhibition, respectively, of acetylcholine release
727 The most characteristic attributes of these neurons were the presence of a low threshold Ca2+ spike."
728 The NMDA responses of two types of feedforward excitatory interneurons in the granular layer, the granule cell and unipolar brush cell (UBC), were compared. A subset of granule cells receive influence from UBC via extrinsic mossy fibers
729 The OFF cone bipolar cells seem dominated by glycinergic input and the ON cone bipolar and rod bipolar cells by GABAergic input
730 The oscillations and the intermittent firing pattern are Ca2+ or SK channel independent, but are completely eliminated by TTX, suggesting that they are due to an interaction between voltage-gated K+ conductances and a persistent or possibly the inactivating sodium conductance responsible for spike generation.”
731 The pharmacologically isolated, GABAergic synaptic currents in bipolar cells were long-lasting (compared with those in in ganglion cells, which are relatively brief). The GABAA receptor component of the bipolar cell response was relatively brief compared with the GABAC receptor component
732 The pharmacology and kinetics of glutamate sensitivity of mitral cells was studied using flash photolysis in rats
733 The physiology of these receptors has been studied in outside-out patches from the proximal apical dendrites. It was found that a CNQX-sensitive component of the synaptic current evoked by fast aplication of glutamate could be isolated (and was presumed to be the result of AMPA channel opening). It was calculated that AMPA channels had a mean elementary conductance of 10 pS (estimated by non-stationary fluctuation analysis) and was found that the channels had a low permeability to Ca2+. The reversal potential for AMPA receptors was found to be about 0 mV with an almost linear peak current-voltage relationship
734 The physiology of these receptors has been studied in outside-out patches from the proximal apical dendrites. It was found that an APV-sensitive component of the synaptic current evoked by fast aplication of glutamate could be isolated (and was presumed to be the result of NMDA channel opening). It was calculated that NMDA channels had a main conductance state conductance of 45 pS and it was confirmed that the channel was permeable to Ca2+. The NMDAR-mediated conductance was blocked by Mg2+ in a voltage-dependent way and by Zn2+ in a non-voltage-dependent fashion
735 The presence of L-channels in all dendritic compartments in mouse motoneurons is supported by electrophysiology and immunehistochemistry
736 The presence of Calcium channels was directly demonstrated by imaging studies
737 The presence of GABAB receptor subtypes BR1 and BR2 on the presynaptic and postsynaptic membranes of GABAergic striatonigral synapses and glutamatergic STN like terminals indicates that besides GABAA, GABAB receptors are also implicated in GABAergic striatonigral transmission."
738 The properties of outward currents were investigated with patch-clamp in acutely isolated cells at various postnatal ages and at adulthood (2-3 mo). Kinetic analysis and pharmacological properties showed that IK and IA were present in these cells. IA and IK remained stable with respect to kinetic properties during ontogenesis, but the relative contribution and pharmacological properties varied with age. IA dominated in P5-7 cells whereas IK was prominent in most older cells
739 The properties of outward currents were investigated with patch-clamp in acutely isolated rat DGCs at various postnatal ages and at adulthood (2-3 mo). Kinetic analysis and pharmacological properties showed that IK and IA were present in these cells. IA and IK remained stable with respect to kinetic properties during ontogenesis, but the relative contribution and pharmacological properties varied with age. IA dominated in P5-7 cells whereas IK was prominent in most older cells
740 The properties of this current have been studied in cell-attached recordings in rats
741 The properties of this current were studied using intracellular recording in slices
742 The properties of voltage-gated potassium currents were studied in acutely isolated rat cells from area CA1 and CA3 at postnatal ages of day 6-8, 9-14, and 26-29 (P6-8, P9-14, and P26-29) with the use of the whole cell version of the patch-clamp technique. In CA1 cells IK was blocked by TEA at +30 mV with an IC50 of 0.98 mM. In CA3 cells the corresponding IC50 value was 1.05 mM. About 20% of IK were insensitive to TEA. IK was partially blocked by approximately 30% with 100 microM 4-AP. Mast cell degranulating peptide (100-200 nM) and dendrotoxin (50-300 nM) had no effect on IK. IK was upregulated with increasing postnatal age. This increase in the expression of IK was approximately 300% much larger in CA1 cells than in CA3 cells, with only approximately 50%
743 The rate of NMDAR channel opening was studied in response to depolarisations at different times after brief (1 ms) and sustained (4.6 s) applications of glutamate to nucleated patches from neocortical pyramidal neurons
744 The responses of most retinal ganglion cells are transient because bipolar-to-ganglion cell transmission is truncated after 150 msec by a feedback inhibition to bipolar cell terminals from GABAergic amacrine cells; the feedback inhibition itself must be delayed by approximately 150 msec to allow the initial bipolar-ganglion cell transmission. One source of the delay appears to be glycinergic amacrine cells to GABAergic amacrine cells to bipolar cell terminals. Results suggest that, after a light flash, a population of glycinergic amacrine cells responds first, inhibiting a population of GABAergic amacrine cells for approximately 150 msec. The GABAergic amacrine cells feed back to bipolar terminals, only after the 150 msec delay, thus allowing the bipolar terminals to excite ganglion cells for the first 150 msec.
745 The reversal potential as well asthe complete blockade of the striatal-evokedsynaptic events by bicuculline or picrotoxin indicatethat neurotransmission between striatonigralfibers and SNr cells is due to activation of GABAAreceptors with chloride ions as charge carriers"
746 The rod-dominant ON-type bipolar cells and some bipolar cells with a small axon terminal receive negative feedback inputs from GABAergic amacrine cells
747 The role of large-conductance Ca2+-dependent K+ channels (BK) in spike broadening during repetitive firing was studied using sharp electrode and computer modelling. The amplitude of the fast after-hyperpolarization (fAHP) rapidly declined during each train. Suppression of BK-channel activity with the selective BK-channel blocker iberiotoxin, the non-peptidergic BK-channel blocker paxilline, or calcium-free medium, broadened the 1st spike to a similar degree ( approximately 60 %)
748 The Schaeffer collateral/commissural pathway elicits EPSPs in CA1 that have a large AMPA receptor-mediated component that can be blocked by CNQX
749 The Schaeffer collateral/commissural pathway elicits EPSPs in CA1 that have an NMDA-receptor mediated component that can be blocked by APV under certain experimental circumstances (such as low bath Mg+ levels). Many authors have suggested that NMDA receptors may be involved in long-term potentiation in this region. (Reviewed in
750 The subcellular distribution and biophysical properties of this current were studied in cell-attached patches. The basal dendrites were practically devoid of this conductance
751 The subcellular distribution and biophysical properties of this current were studied in cell-attached patches. Up to approximately 400um from the soma a low density of channels was found, with a 20-fold increase in the apical distal dendrite. The findings suggest that integration of synaptic input to the apical tuft and the basal dendrites occurs spatially independently due to the high Ih channel density in the apical tuft that increases the electrotonic distance between these two compartments in comparison to a passive dendrite
752 The subthalamic nucleus (STN) receives a dopaminergic innervation from the substantia nigra pars compacta.”
753 The transient voltage-gated sodium current is strong and fast in SNr GABA neurons. When a sufficient amount of the classical INaT is activated by subthreshold depolarization induced by TRPC3 channels and INa,p [persistent], the regenerative fast rising phase of the action potential is triggered ”
754 The vast majority of Nav1.1 labeling in axons was specifically localized at myelinated portions of the axon. Consistent with previous observations, Nav1.2 was found mainly in small unmyelinated axons and Nav1.6 was specifically associated with nodes of Ranvier. A low level of labeling for each type of sodium channel was also found in axon terminals.”
755 The way that different parts of a neuron carry out multiple information processing roles is illustrated by the CA1 pyramidal cell in the hippocampus. The authors used 2-photon microscopy to obtain high resolution images of calcium signals in the apical dendrites while activating Schaffer collateral inputs to induce long-term potentiation (LTP) of different durations. Short-duration LTP (LTP 1) was associated with Ca increase in dendritic spines, due to activation of NMDA receptors and local ryanodine receptors (RyRs). Intermediate duration LTP (LTP 2) was associated with Ca increase in dendritic branches, due to activation of NMDA receptors and local IP3 receptors (IP3Rs). For Ca increase in long duration LTP (LTP3), see Ca channels in CA1 pyramidal cell apical dendrite. ...
756 There is a selective localization of GABA receptors at symmetric synaptic junctions and of glutamate receptors at asymmetric junctions
757 There is also evidence that Zn+ can modulate bicuculline-sensitive responses to GABA early in development in rat (studied less than 8 days old)
758 There is no synaptic inhibition in this cell
759 These channels "prevent initiation of an action potential in the dendrites, limit the backpropagation of action potentials into the dendrites, and reduce excitatory synaptic events"
760 These channels are assembled from subunits of the Kv3 family and are necessary for the fast spiking phenotype of O/A interneurons
761 These factors all point to Kv2 family channels as being responsible for the slowly deactivating, slowly inactivating delayed rectifier in GP neurons."
762 These factors may contribute to greater susceptibility of endopiriforn nucleus to epileptogenesis. Reviewed in
763 These results suggest that serotonergic afferents from raphe dynamically modulate olfactory processing through distinct effects on multiple OB targets, and may alter the degree to which OB output is shaped by inhibition during behavior.
764 This channel is present in high density in all species. Original intracellular recordings suggesting site of impulse initiation is the axon hillock with backspread into the soma dendrites
765 This conductance triggers impulses in dendrites and soma, leading to Ca-dependant K conductances
766 This current "may be of limited significance within the normal physiological range of potential and extracellular environment"
767 This current is inactivated at rest and de-inactivated by hyperpolarization; sequences of hyperpolarization-depolarization therefore activate I A, producing the pauser reponse
768 This current is reduced by activation of the metabotropic glutamate receptors
769 This current was measured in nucleated patches from O/A interneurons and found to be ~19% of the total potassium current
770 This current was studied by combining intracellular recordings and two-photon microscopy imaging of [Ca]i
771 This current was studied using whole-cell and perforated patch-clamp in O/A interneurons
772 This is fast activating. There is also I P which is A-like but slowly activating. Some kinetic properties of this current were studied in cell-attached recordings in rats
773 This is only observed in rods in salamander.
774 This is the non-selective Na and K current located in the plasma membrane of the distal segment. It is activated in the dark by cyclic GMP from the disc membranes.
775 This is the non-selective Na and K current located in the plasma membrane of the distal segment. It is activated in the dark by cyclic GMP from the disc membranes.
776 This persistant conductance may be activated by the NMDA receptor depolarization, providing a mechanism for graded, voltage dependent EPSP amplification
777 Three types of glutamate receptors for 1) cone-activated receptors of HCs; 2) cone-activated receptors of OFF-BPs; and 3) rod-activated receptors found in HCs and BPs
778 Thus there is a steady-state calcium current contributing to the depolarization phase of the oscillation but small in comparison with the sodium current."
779 Tonically active at rest; induces a sag in hyperpolarizing responses; blocked by ACh.
780 Transients and kinetics for these channels were studied using whole-cell patch clamp recordings
781 TTX-resistant
782 TTX-sensitive
783 TTX-sensitive sodium current (possibly of the transient type?) may also be present
784 Two soluble guanylyl cyclases have been cloned and expressed
785 Two types of A-like current were observed in GP neurons: a high-threshold, TEA-sensitive current attributable to Kv3.4 channels and a low-threshold, TEA-insensitive current attributable to Kv4 family channels.”
786 Two types of PG cells can be distinguished by the presence of delayed-rectifier. R-type has DR current and shows outward rectification under current-clamp; N-type does not. A third type, X-type, has properties of both R- and N-type. Zinc modifies the A-type current, but not the delayed-rectifier type: at given voltages, it reduces A-current peak amplitude, slows its kinetics. Zinc shifts activation and inactivation toward more positive voltage. Thus, at physiological resting potential -55mV, zinc accelerates repolarization.
787 Type 1 synapse
788 Types and distribution of voltage-gated K+ channels in the soma and apical dendrites were studied in acute brain slices
789 Unlike postsynaptic NMDAR's, they are potentiatedby physiologically relevant concentrations of taurine
790 Unlike the retinogeniculate input, the corticogeniculate input is received by both ionotropic and metabotropic glutamate receptors
791 Unpublished data by Chen and Shepherd have revealed a long lasting after hyperpolarization following a train of action potentials. Using whole-cell recordings, the kinetic properties of this current have been investigated in neurones from neonatal rats, which were retrogradely labelled and identified after enzymatic dissociation
792 Using a monoclonal antibody
793 Using a whole chick (Gallus domesticus) basilar papilla preparation, a map of changes in potassium currents of tall hair cells was produced. All cells recorded from expressed IKCa and IK. The amplitude of total outward current increased in a gradient along the tonotopic axis
794 Using a whole chick (Gallus domesticus) basilar papilla preparation, it was found that apical cells expressed I-IR
795 Using Ca2+ imaging, full action potential invasion throughout the length of the basal dendrites, suggesting the presence of Na channels at somatic density, was observed by
796 Using Ca2+ imaging, full action potential invasionthroughout the length of the basal dendrites, suggesting the presence ofNa channels at somatic density, was observed by
797 Using calcium imaging, calcium waves in layer 2/3 and layer 5 neocortical somatosensory pyramidal neurons were examined in slices from 2- to 8-week-old rats
798 Using confocal microscopy, these channels were found to be localized on the soma, dendrites, and a subpopulation of dendritic spines
799 Using conventional or perforated-patch whole cell recordings, SNc neurons acutely dissociated from P4 to P16 rats NMDA (100 nM, V(hold) = -60 mV) evoked inward, APV-sensitive currents (56.4 +/- 8.6 pA) in all tested neurons (n = 29). Strong depolarizing responses were observed under current-clamp
800 Using differential polarization through applied electric fields, cell bodies and dendrites have been activated in effective isolation during intracellular recordings in vitro. In neurons located in the rostral substantia nigra, the dendrites are shown to have both HVA and LVA channels. HVA conductance appears to be exclusively dendritic. By contrast, in more caudally located cells HVA calcium spikes were located principally in the cell body
801 Using double-staining techniques, the distribution of NADPH-diaphorase (ND)- and nitric oxide synthase (NOS)-positive cells was compared in the periglomerular region of typical and atypical rat olfactory glomeruli. The number of ND/NOS-stained periglomerular cells was much higher (P &lt 0.001) in typical than in atypical glomeruli.
802 Using electrophysiological recordings and imaging, the density of these channels was found to rapidly decrease with distance from soma
803 Using electrophysiological recordings and imaging, the density of these channels was found to rapidly decrease with distance from soma and clustered in high density around the base of dendrites
804 Using ex vivo slices of guinea pig midbrain, we show that SNr GABAergic neurons express transient receptor potential melastatin 2 (TRPM2) channels that underlie NMDA-induced burst firing. Furthermore, we show that spontaneous firing rate and burst activity are modulated by the reactive oxygen species H(2)O(2) acting via TRPM2 channels. Thus, our results indicate that activation of TRPM2 channels is necessary for burst firing in SNr GABAergic neurons and their responsiveness to modulatory H(2)O(2).”
805 Using ex vivo slices of guinea pig midbrain, we show that SNr GABAergic neurons express transient receptor potential melastatin 2 (TRPM2) channels that underlie NMDA-induced burst firing. Furthermore, we show that spontaneous firing rate and burst activity are modulated by the reactive oxygen species H2O2 acting via TRPM2 channels. Thus, our results indicate that activation of TRPM2 channels is necessary for burst firing in SNr GABAergic neurons and their responsiveness to modulatory H2O2.”
806 Using in vitro methods, the modulatory actions of 5HT were examined on three different calcium-insensitive K-currents among others
807 Using intra- and extracellular recordings in ferret it has been shown that these neurons interact locally through the activation of GABA-A receptor-mediated inhibitory potentials
808 Using outside-out patches and a fast application system the properties and distribution of synaptic glutamate receptors an approximately twofold increase in AMPA-mediated current was observed in the dendritic region that receives a uniform density of Schaffer collateral input (100-250um from soma)
809 Using radioactive in situ hybridization methods, heavy labeling for NMDAR1 subunit was observed in all major CN neuronal types with lower labeling for NMDAR2A, 2B, 2C, and 2D mRNA
810 using whole-cell patch-clamp recordings from freshly dissociated mouse neocortical pyramidal neurons showed that Ca2+-dependent K+ currents were activated by Ca2+ entry through both N- and L-type channels
811 Using whole-cell recordings, the kinetic properties of this current have been investigated in neurones from neonatal rats, which were retrogradely labelled and identified after enzymatic dissociation
812 Variable densities of active channels support variable extents of backpropagating impulse in the dendrites
813 Voltage-clamp analysis suggested that IAHP in DG neurones is generated by about 1200 channels, and that about 60% are open at the peak of a maximal IAHP
814 Voltage-dependent Ca currents are seen in isolated bipolar cells
815 Voltage-gated sodium channels were found throughout the whole dendritic tree of GP neurons, and showed a significant clustering at sites of excitatory synaptic inputs.”
816 Voltage-sensitive dye signals recorded from the glomerular layer reflect activity in periglomerular cells and that Cl- efflux through non-GABAA chloride channels contributes to the postsynaptic depolarization of these cells after olfactory nerve stimulation
817 We find that small-conductance Ca2+-activated K+ (SK) channels underlie most of the mAHP in GP neurons. This mAHP conductance is a small component of the overall outward current that flows during the subthreshold part of the oscillatory cycle, the majority of which is provided instead by an inactivating K+ current."
818 Whereas, activation of the adenosine A1 receptor reduces synaptic strength by modulating presynaptic calcium channels, baclofen modulates presynaptic calcium channels as well, but also affects release processes downstream from calcium entry
819 which is important for the induction of long term changes in synaptic strength"
820 While nicotinic and muscarinic acetylcholine receptors exist in FSI-SPN synapses, only the nicotinic receptors are postsynaptic.
821 While NMDA receptor activation may be necessary for LTP at the commissural/associational synapses
822 Whole cell and perforated patch recordings in slices showed bicuculline-dependent and ?independent GABA currents from juvenile rats, suggesting two types of GABAergic inputs. The bicuculline-independent component was present only at the earliest stages of maturation, had a later peak, slower time course of decay, and marked outward rectification. A trophic or signaling role rather than primarily inhibitory was suggested for this current
823 Whole cell recording experiments have revealed a sustained, partially nimodipine-sensitve current in steps to -50mV, suggesting that they play a role in CA2+ signalling at low voltages as well as a their classical high voltages
824 Whole cell recording experiments have revealed a sustained, partially nimodipine-sensitve current in steps to -50mV, suggesting that they play a role in CA2+ signalling at low voltages as well as a their classical high voltages
825 Whole cell recording from acutely isolated rat CA3 pyramidal neurons revealed a transient (59 msec decay time constant) that was inhibited by Ni2+ and amiloride
826 Whole cell recordings from acutely dissociated neurons exhibited a R-type currents that were characterized as HVA by their rapid deactivation kinetics, half-activation and half-inactivation voltages, and sensitivity to depolarized holding potentials. In neocortical pyramidal neurons these currents inactivated at more negative potentials than in medium spiny neurons
827 Whole-cell and cell-attached patch-clamp recordings showed that ACh activates apamin-sensitive, "SK"-type potassium channels
828 Whole-cell patch-clamp recording of ICa from presynaptic boutons are comparable to that obtained from somatic recordings, but elevation of intracellular Ca is restricted to the presynaptic terminals, with no somatic or axonal changes observed
829 Whole-cell patch-clamp recordings showed that variations in the kinetics of the outward current contribute substantially to the determination of resonant frequency
830 Whole-cell patch-clamp recordings were used to identify and characterize ionic currents in isolated cells. All hair cells possessed an IKCa
831 Whole-cell patch-clamp recordings were used to identify and characterize ionic currents in isolated cells. In a small subset of cells, the IK was replaced by an IA. It is suggested that the kinetic properties of the ionic currents argue against electrical tuning
832 Whole-cell patch-clamp recordings were used to identify and characterize ionic currents in isolated cells. Most cells possessed a slowly activating IK, which is approximately 80% inactive at rest. In a small subset of cells, IK was replaced by an IA. It is suggested that the kinetic properties of the ionic currents argue against electrical tuning
833 Whole-cell patch-clamp recordings were used to identify and characterize ionic currents in isolated cells. Most cells possessed an Ih, which actively contributed to the resting potential
834 Whole-cell somatic recording during TTX application to proximal dendrites suggests the presence of a persistent Na current
835 Whole-cell voltage-clamp recordings showed that a low-threshold transient (T-type) Ca2+ current was observed in 40% of neurons
836 Whole-cell voltage-clamp recordings showed that HVA currents were present in at least 95% of neostriatal neurons, but that the majority of them appeared to belong neither to the "L-type" nor the "N-type" classification
837 With a postembedding immunogold procedure, it has been found that these receptors do not appear to be concentrated in clusters on dendrites, suggesting that the presynaptic effects of glutamate are mediated by a small complement of extrasynaptic receptors
838 With whole-cell patch clamp, two types of A-current were found in rat neostriatal neurons, one similar to previous descriptions in mammals and a second activated at considerably more depolarized potentials
839 With whole-cell recordings the properties of a voltage-dependent Na+ currents were investigated in 42 DGC acutely isolated from the resected hippocampus of 20 patients with therapy-refractory temporal lobe epilepsy (TLE) using the whole-cell patch-clamp technique.The kinetic properties contributed to a reduction of the Na+ currents during repetitive stimulation that was more pronounced with higher stimulation frequencies and also showed a dependence on the holding potential
840 Young and Oertel, in
841 Zn2+ modulates the inhibitory interaction between amacrine and bipolar cells, particularly that mediated by the GABA(C) receptor