Publication facts - List

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).