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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