ライフサイエンスコーパス: IPSP

1 IPSP duration was shorter at physiological temperature t

2 IPSP/Cs could only rarely be elicited in spiny projectio

3 IPSPs are mediated by small rebound spikes, which are gr

4 IPSPs were blocked by the Cl(-) channel blocker picrotox

5 IPSPs were composed of both slow, sustained components a

6 IPSPs were GABAergic, because they reversed at the chlor

7 IPSPs were sensitive to bicuculline (10 microM) in all n

8 IPSPs, elicited by synaptic input from a presynaptic LN,

9 urces of inhibition were present in AN1: (1) IPSPs were elicited by stimulation with 12.5 kHz stimuli

10 ndicate that CGRP increases ST-evoked GABA-A IPSPs and hyperpolarizes their reversal potential throug

11 cilitation of monosynaptic medial B-medial A IPSPs and intrinsic changes in excitability of type A an

12 paired-pulse facilitation of evoked GABA(A) IPSPs and IPSCs and always increased the frequency and s

13 ol increased the amplitude of evoked GABA(A) IPSPs and IPSCs in 70% of CeA neurons.

14 ethanol potentiation of hippocampal GABA(A) IPSPs and IPSCs, suggesting that some unknown GABA(B) re

15 In addition, GABA(A) IPSPs evoked by stimulation of the external capsule were

16 the resistance drop associated with GABA(A) IPSPs was not altered.

17 Local stimulation also elicited GABA(A) IPSPs, at least some of which arose from identified spin

18 ability and decreasing the impact of GABA(A) IPSPs.

19 zepine diazepam enhances the size of GABA(A) IPSPs; its effects are reversed by the antagonist flumaz

20 ated cation current, I(H), which accelerated IPSP decay over a broad range of membrane potentials and

21 ng but were indeed transiently boosted after IPSPs.

22 Consequently, after IPSPs, Ca signals return to baseline, although firing is

23 rrent, I(NaP), which prolonged and amplified IPSPs at depolarized subthreshold potentials.

24 Only the post-POC amplitude IPSPs elicited the POC-triggered activity pattern in thi

25 ptic responses consisted predominantly of an IPSP at low stimulation frequency (0.05 Hz).

26 In most cases, EPSP and IPSP frequencies were not affected by temperature change

27 s suggest an overlap in time of the EPSP and IPSP, with a small drop in input resistance and an appar

28 orporated short-term plasticity of EPSPs and IPSPs and slow IPSPs.

29 es and widths at half-amplitude of EPSPs and IPSPs and the EPSP paired pulse ratio.

30 ation of the solitary tract evoked EPSPs and IPSPs in DVN neurons and BDS increased the average ampli

31 he characteristics of the recorded EPSPs and IPSPs reveal that IPSPs are important in controlling the

32 in silent cells where both evoked EPSPs and IPSPs were present.

33 CN may be driven by bursts of both EPSPs and IPSPs, and may result in persistent changes to both firi

34 rical stimulation of the TS evoked EPSPs and IPSPs, and TEA and 4-AP increased the average amplitude

35 IPSCs and IPSPs were elicited by electrically stimulating the cort

36 neous excitatory postsynaptic potentials and IPSPs that remain in the presence of tetrodotoxin.

37 studied temporal integration of simEPSCs and IPSPs at P15.

38 le or revealed an evoked IPSP (200 nM ANGII: IPSP conductance increased from 70 +/- 29 to 241 +/- 34

39 Blocking both the GABA(B) IPSP and sAHP simultaneously eliminated the effect of el

40 Antagonism of the GABA(B) IPSP and/or sAHP diminished stimulus-induced hyperpolari

41 ent inhibition of gamma-aminobutyric acid(B) IPSPs in dopamine neurons was present in wild-type anima

42 g hyperpolarization mediated through GABA(B) IPSPs and sAHP.

43 so blocked the isolated synchronized GABA(B) IPSPs generated in CA3 cells by a subpopulation of inter

44 relay neurons, where instead robust GABA(B) IPSPs occurred.

45 the amount of GABA released because GABA(B) IPSPs were unchanged and the resistance drop associated

46 y CGRP, and there was no correlation between IPSP potentiation and variance, suggesting that CGRP act

47 burst firing patterns activated the broadest IPSPs and received the slowest, most strongly facilitati

48 e component of transient sodium current, but IPSP-like waveforms engaged primarily persistent sodium

49 SPs were pronounced at expiratory onset, but IPSPs were not apparent during inspiration, although XII

50 o showed that offset firing was triggered by IPSPs rather than EPSPs.

51 Complex IPSP trains, including spike trains recorded in vivo, dr

52 tional decrease in the amplitude of compound IPSPs recorded in the postsynaptic B photoreceptors.

53 ns using current-clamp recordings containing IPSPs as voltage-clamp waveforms.

54 In connections in which a delayed IPSP occurred, blocking the feedforward inhibition in mo

55 nstrate that the somatic impact of dendritic IPSPs is highly voltage dependent and controlled by clas

56 increased the duration of proximal dendritic IPSPs generated at depolarized potentials and distal den

57 Depolarizing IPSPs (dIPSPs) are kept below spike generation threshold

58 y inputs are integrated and how depolarizing IPSPs affect spike thresholds and synaptic integration b

59 tive shift of reversal potential of IPSPs (E(IPSP)).

60 nhibitory postsynaptic potentials (IPSPs), E(IPSP), in spinal motoneurons, increases the cell membran

61 re attributable to bidirectional shifts of E(IPSP).

62 small, delayed EPSPs preceded by an earlier IPSP and no action potentials in chandelier cells, diffe

63 but only in Gr cells did it reveal an early IPSP that cut short the EPSP.

64 This early IPSP was associated with a large decrease in input resis

65 he hyperpolarizations might be due to either IPSPs or disfacilitation.

66 g membrane potentials where I(h) is engaged, IPSPs produce rebound bursts of action potentials.

67 ute ethanol (5-66 mm) significantly enhanced IPSPs and IPSCs equally in CET and naive rats, indicatin

68 to parallel fiber input with an EPSP or EPSP-IPSP sequence and show only large, narrow spikes in resp

69 n an OFF ganglion cell are caused by an EPSP/IPSP sequence evoked from within the dendritic field; in

70 tial/inhibitory postsynaptic potential (EPSP/IPSP) sequence, with the latter having both a GABA(A) an

71 e they were detectable or revealed an evoked IPSP (200 nM ANGII: IPSP conductance increased from 70 +

72 eA slices from CET rats, the baseline evoked IPSP and IPSC amplitudes were increased, and paired-puls

73 D-Lys3-GHRP-6 and JMV 3002 decreased evoked IPSP and mIPSC frequency, revealing tonic ghrelin activi

74 ANGII either increased TS-evoked IPSP conductances in cells where they were detectable or

75 ease in EPSPs but had no effect on TS-evoked IPSP potentiation by ANGII.

76 CPA did not affect evoked IPSPs.

77 d dendrite, where recurrent EPSPs and evoked IPSPs were largely suppressed.

78 ine (Rp-cAMPs), none of which blocked evoked IPSPs.

79 oM) reversibly increased electrically evoked IPSPs in 5/10 rostral NTS (rNTS) neurones but only in 2/

80 During these epochs, LN-evoked IPSPs caused phase-locked, population oscillations in se

81 ced by 26% the mean amplitude of NRGc-evoked IPSPs (1.9+/-0.2 mV (S.E.M.) vs. 1.4+/-0.2 mV; n=11, con

82 ides have a modulatory effect on NRGc-evoked IPSPs during carbachol-induced motor inhibition.

83 Although the conductances of evoked IPSPs recorded in normal ACSF were not significantly red

84 as that seen for the polysynaptically evoked IPSPs.

85 ST-evoked IPSPs, also detected at E16, were eliminated by GABA(A)

86 n in both spontaneous and stimulation-evoked IPSPs, leading to a hyperexcitability of the BLA network

87 plied GABA, the effect of ANGII on TS-evoked IPSPs may occur presynaptically.

88 These excitatory IPSPs can directly trigger low-threshold spikes (LTSs).

89 ependent of the decrease of the f-EPSP and f-IPSP, because PKC antagonists block the increase in PKC

90 he mechanism that decreases the f-EPSP and f-IPSP.

91 reases a bicuculline-sensitive field-IPSP (f-IPSP), and this occurs whether the f-EPSP is potentiated

92 o not block ACPD's effect on the f-EPSP or f-IPSP.

93 ate (group I mGluR agonist), decreases the f-IPSP, and increases PKA activity, suggesting that the in

94 mGluRs) decreases both the f-EPSP and the f-IPSP, but increases PKC and PKA activity.

95 B34, are GABA-immunoreactive and evoke fast IPSPs in their postsynaptic followers.

96 eased histamine, in addition to evoking fast IPSPs in OX cells, mediates a prolonged decrease in exci

97 The fast IPSPs were blocked by the GABAA receptor chloride channe

98 uptake inhibitors, we found that these fast IPSPs are likely mediated by GABA.

99 Functionally, these fast IPSPs specify two parameters for ingestive motor program

100 urons respond to single TM stimuli with fast IPSPs, whose kinetics resemble those of GABA(A) or glyci

101 netics followed by trains of smaller, faster IPSPs.

102 nes with narrow spikes generated the fastest IPSPs in pyramidal cells and received the briefest, most

103 influence of dynamic-clamp-injected feedback IPSPs of pre- and post-POC amplitude into a pivotal proj

104 ity-dependent development of the feedforward IPSP.

105 Onsets of feedforward IPSPs coincided with the rising phase of the pyramidal c

106 tion decreases a bicuculline-sensitive field-IPSP (f-IPSP), and this occurs whether the f-EPSP is pot

107 loss of both field theta and theta frequency IPSP trains.

108 Thus, high-frequency IPSPs in cerebellar nuclear neurons evoke little postinh

109 ibition, which accompanies the classic GABAA IPSP.

110 r than decreased, the amplitude of the GABAB IPSP.

111 outlast the underlying CS-mediated GABAergic IPSP.

112 wed that the interneurons elicited GABAergic IPSPs/IPSCs in spiny neurons powerful enough to signific

113 Finally, isolated GABAergic IPSPs between inhibitory and excitatory neurons could be

114 ons, we observed fast monosynaptic GABAergic IPSPs in the majority (>60%) of fast-spiking (FS) and lo

115 in an increase in the amplitude of GABAergic IPSPs in both input pathways.

116 requency (10 Hz), the amplitude of GABAergic IPSPs was maintained, and spike output from LTS and FS i

117 xin caused a slow enhancement of glycinergic IPSPs and transient lateral inhibition produced by a rot

118 essed when preceded by simulated glycinergic IPSPs.

119 resistance, can still fire briskly and have IPSPs superimposed on the slow GABAergic depolarization,

120 Hilar IPSPs have low failure rates, are blocked by the GABA(A)

121 However, IPSP paired-pulse ratios were unchanged by CGRP, and the

122 However, IPSPs could themselves elicit action potentials, and fac

123 However, IPSPs during ETX displayed a significantly greater sensi

124 nhibitory than conventional, hyperpolarizing IPSPs in the same neurons.

125 and the tap US also produced hyperpolarizing IPSPs.

126 xpiratory-phased IPSCs without any change in IPSP frequency.

127 stimulation of the MNTB led to a decline in IPSP amplitude by 43%.

128 he magnitude of ghrelin-induced increases in IPSP amplitude was not significantly different from that

129 did not affect ethanol-induced increases in IPSP amplitude.

130 hane depressed EPSP amplitudes and increased IPSP amplitudes recorded from both types of neurons.

131 plied alone, ethanol significantly increased IPSP amplitude, but this effect was attenuated by the ap

132 e application of CRF significantly increased IPSPs in the CeA, and this enhancement was blocked by N/

133 cocaine, which blocks 5-HT uptake, inhibited IPSPs in the dorsal raphe and the ventral midbrain of wi

134 inhibitory synaptic potentials with initial IPSPs with slow kinetics followed by trains of smaller,

135 Interestingly, IPSPs modified action potentials (APs) in a manner that

136 occluded the GABA(B)-receptor-mediated IPSP (IPSP(B)) which preceded it.

137 from inhibition through integration of large IPSPs, driven by an extremely negative chloride reversal

138 It is concluded that the large IPSPs with slow rise-times that are observed in motoneur

139 was readily detected, comprising much larger IPSPs.

140 trigeminal nucleus produced shorter latency IPSPs.

141 ) and occluded the GABA(B)-receptor-mediated IPSP (IPSP(B)) which preceded it.

142 rophysiological recordings of GABAA-mediated IPSPs in the central nucleus of the amygdala (CeA) to ex

143 ute presynaptic inhibition of GABAB-mediated IPSPs by mu- and kappa-opioid receptors and the effects

144 botropic glutamate receptor (mGluR)-mediated IPSPs in dopamine neurons, but has no effect on ionotrop

145 ages of GABA(A) receptor (GABA(A)R)-mediated IPSPs arising from pallidal fibers.

146 e ethanol augments GABA(A) receptor-mediated IPSPs and IPSCs, possibly by a presynaptic mechanism.

147 s and deactivated by GABAA receptor-mediated IPSPs.

148 These mGluR IPSPs are caused by release of Ca(2+) from intracellular

149 lls from epileptic rats, evoked monosynaptic IPSP conductances were <40% of controls, and the frequen

150 as a comparable decrease in the monosynaptic IPSP conductances examined in the presence of glutamater

151 stimulation of the CAA elicited monosynaptic IPSPs in SPNs located laterally in the intermediolateral

152 s of pharmacologically isolated monosynaptic IPSPs, IPSCs and inhibitory conductances (g GABAA), show

153 evoked GABAA receptor-mediated monosynaptic IPSPs in deep cerebellar nuclei neurons by stimulation o

154 No monosynaptic IPSPs could be recorded in the presence of gabazine, sho

155 Moreover, IPSPs mediated by single Golgi cell action potentials pa

156 showed a transition from fast (100-150 msec) IPSPs to slow ( approximately 300 msec) IPSPs.

157 sec) IPSPs to slow ( approximately 300 msec) IPSPs.

158 activation of BFc axons elicited muscarinic IPSPs.

159 above approximately 6-8 Hz, these muscarinic IPSPs lost their efficacy because stimulation of BFc inp

160 In three neurones IPSPs evoked by stimulation of the iLF (n = 1) or cLF (n

161 nts from area X evoked a strong, all-or-none IPSP whose amplitude and latency were unchanged by appli

162 L-1beta or IL-6 suppressed the noradrenergic IPSPs and the fast EPSPs, and the two acted synergistica

163 myenteric projections and with noradrenergic IPSPs evoked by sympathetic fibres that innervated the s

164 In contrast, EPSPs but not IPSPs were recorded after adding strychnine with gabazin

165 When the observed IPSP arrival times were analyzed as a superposition of r

166 The analysis of IPSP arrival times as a superposition of renewal process

167 Application of IPSP bursts evoked a large number of rebound spikes and

168 reas long-lasting depression or no change of IPSP amplitude was likely to be observed in neurons that

169 increased the ghrelin-induced enhancement of IPSP amplitude, but to a lesser extent than ethanol alon

170 trical coupling but reduced the amplitude of IPSPs and IPSCs between FS cells.

171 ure had opposite effects on the amplitude of IPSPs and IPSCs.

172 BNST-AL cells but increased the amplitude of IPSPs evoked by stimulation of the stria terminalis (ST)

173 g amplitudes of spikes against amplitudes of IPSPs has a characteristic S shape with a linear central

174 kinetics, and dendro-somatic attenuation of IPSPs generated from depolarized (-50 mV) and hyperpolar

175 ell as reversed, CRF-induced augmentation of IPSPs, actions that required PKA signaling.

176 While the earliest components of IPSPs and EPSPs evoked by group II afferents were abolis

177 The reversal potentials and conductances of IPSPs in granule cells in epileptic versus control gerbi

178 ctionally, this voltage-dependent control of IPSPs shaped the spatial and temporal profile of inhibit

179 At the soma, the time course of IPSPs evoked from depolarized potentials was greatest wh

180 distally, whereas the somatic time course of IPSPs evoked from hyperpolarized potentials was independ

181 in duration but strong voltage dependence of IPSPs arising from somatic and dendritic synapses.

182 The potentiation or depression of IPSPs was associated with a negative or positive shift o

183 c agonist pilocarpine mimicked the effect of IPSPs on MC maximal firing rate, and action potential he

184 The ethanol enhancement of IPSPs and IPSCs occurred to a similar extent in the pres

185 licit action potentials, and facilitation of IPSPs by repetitive activation could lead to a character

186 shold either single or bursts (10-100 Hz) of IPSPs gave rise to a rebound excitation and action poten

187 ted and N/OFQ exerted a larger inhibition of IPSPs compared with unrestraint rats.

188 ons, where location-specific interactions of IPSPs with voltage-activated ion channels are likely to

189 The modifications of IPSPs were dependent on activation of postsynaptic volta

190 Pharmacological modulation of IPSPs altered the theta oscillation suggesting an inhibi

191 Potentiation of evoked EPSPs, but not of IPSPs, involves activation of NK1 receptors.

192 Functionally, increasing the number of IPSPs markedly lengthened the period of spike inhibition

193 We show experimentally that the polarity of IPSPs contributes to their efficacy; dIPSPs induce accom

194 e or positive shift of reversal potential of IPSPs (E(IPSP)).

195 We found that long-lasting potentiation of IPSPs could be induced in the neurons exhibiting three o

196 fferences were observed in the proportion of IPSPs and EPSPs between control and gabazine conditions.

197 We tested the susceptibility of IPSPs and EPSPs evoked from group II afferents in contra

198 gration of single or low-frequency trains of IPSPs and autonomous activity.

199 ing and were temporally related to trains of IPSPs with slow kinetics.

200 During 50 Hz trains of IPSPs, firing was initially interrupted, but resumed coi

201 perpolarizing current disclosed two types of IPSPs in response to the tap US.

202 ratio and in the coefficient of variation of IPSPs, consistent with decreased GABA release probabilit

203 orsal thalamic nuclei evokes robust IPSCs or IPSPs in other specific dorsal thalamic nuclei and vice

204 e disinhibited during the interictal period, IPSPs were recorded in vivo with hippocampal circuits in

205 nge in the initial slope of the postsynaptic IPSP in the A photoreceptor, suggesting that spike durat

206 ll action potentials and on the postsynaptic IPSP in the A-cell was occluded by previous paired (but

207 d an EPSP-inhibitory postsynaptic potential (IPSP) complex.

208 muli, the inhibitory postsynaptic potential (IPSP) conductance and the responses to a 10 Hz, 10 s sti

209 that the inhibitory postsynaptic potential (IPSP) is abolished before the excitatory postsynaptic po

210 and slow inhibitory postsynaptic potentials (IPSPs) (53% and 66%, respectively).

211 mediated inhibitory postsynaptic potentials (IPSPs) and currents (IPSCs) in most CeA neurons, with a

212 ntaneous inhibitory postsynaptic potentials (IPSPs) and currents (IPSCs) were usually blocked with pe

213 f evoked inhibitory postsynaptic potentials (IPSPs) and the frequency of miniature inhibitory postsyn

214 synaptic inhibitory postsynaptic potentials (IPSPs) between acute hippocampal slices from Ts65Dn mice

215 revealed inhibitory postsynaptic potentials (IPSPs) between RE cells that reversed and became depolar

216 mediated inhibitory postsynaptic potentials (IPSPs) by decreasing GABA release and prevented, as well

217 riven by inhibitory postsynaptic potentials (IPSPs) imposed by GABAergic granule cells.

218 synaptic inhibitory postsynaptic potentials (IPSPs) in 75% and 65% of SPNs, respectively.

219 ng giant inhibitory postsynaptic potentials (IPSPs) in CA3 pyramidal cells.

220 cinergic inhibitory postsynaptic potentials (IPSPs) in cat motoneurons.

221 Inhibitory postsynaptic potentials (IPSPs) in ICd neurons evoked in both normal and ETX rats

222 ABAergic inhibitory postsynaptic potentials (IPSPs) in intraspinal stretch receptor neurons (edge cel

223 ted slow inhibitory postsynaptic potentials (IPSPs) in the dorsal raphe of wild-type but not knockout

224 times of inhibitory postsynaptic potentials (IPSPs) observed in intracellular recordings from cat spi

225 presumed inhibitory postsynaptic potentials (IPSPs) that were larger in amplitude and more rhythmic t

226 ensitive inhibitory postsynaptic potentials (IPSPs) when recorded in dopaminergic cells.

227 s evoked inhibitory postsynaptic potentials (IPSPs), and stimulation of cholinergic axons evoked nico

228 ntial of inhibitory postsynaptic potentials (IPSPs), E(IPSP), in spinal motoneurons, increases the ce

229 ing late inhibitory postsynaptic potentials (IPSPs), slowing heart rate and modulating hormone releas

230 rneurone inhibitory postsynaptic potentials (IPSPs), studied with dual intracellular recordings, had

231 specific inhibitory postsynaptic potentials (IPSPs).

232 mediate inhibitory postsynaptic potentials (IPSPs).

233 SPs) and inhibitory postsynaptic potentials (IPSPs).

234 latency inhibitory postsynaptic potentials (IPSPs).

235 GABA(B) inhibitory post-synaptic potentials (IPSPs) or slow after-hyperpolarization (sAHP).

236 Presumed inhibitory synaptic potentials (IPSPs) recorded from principal cells were more rhythmic

237 zed, as during a burst of action potentials, IPSPs produce classic inhibition.

238 ating the laryngeal nerve elicited primarily IPSPs in premotor neurons that could be blocked by a nic

239 As the oscillation progresses, IPSPs recover and slow the neuronal firing to beta frequ

240 h IPSP frequency, and the timing of Purkinje IPSPs and nucleo-olivary spikes was uncorrelated.

241 rop during 500 ms, 100 Hz trains of Purkinje IPSPs or hyperpolarizing steps.

242 tivation of muscarinic receptors, long-range IPSPs were presynaptically inhibited by M2 receptor acti

243 in the brain slice preparation, we recorded IPSPs from STN neurons during electrical stimulation of

244 Onsets of recurrent IPSPs did not occur during the rising phase of the evoke

245 ntaining serotonin, which is known to reduce IPSPs in this preparation.

246 oad range of membrane potentials and reduced IPSP amplitudes at hyperpolarized potentials, and the pe

247 LFP spikes were correlated with the rhythmic IPSP activities recorded within the thalamic ventral pos

248 To investigate this, we simulated IPSPs as a conductance source at sites across the somato

249 In contrast to the slow IPSP, the amplitude of the cholinergic fast excitatory p

250 -term plasticity of EPSPs and IPSPs and slow IPSPs.

251 Synaptically released glutamate evokes slow IPSPs mediated by metabotropic glutamate receptors (mGlu

252 ting (approximately 10 sec) feedforward slow IPSPs (sIPSPs) in RT cells, which were mimicked and bloc

253 ceptor antagonist CGP 35348 blocked the slow IPSPs and converted the 3-4 Hz paroxysmal oscillations b

254 e inhibitory interneurons that produce small IPSPs with fast rise-times during quiet sleep are also r

255 s that mediated site independence of somatic IPSP time course at hyperpolarized potentials.

256 Somatic IPSPs, dendritic burst firing and stratum pyramidale int

257 vidence that the large active sleep-specific IPSPs are comprised of a small number of minimal unitary

258 termingled with larger active sleep-specific IPSPs with 10-90% rise-times > or = 1.00 ms and amplitud

259 arge amplitudes of the active sleep-specific IPSPs, we suggest that each source is a cluster of synch

260 or the large amplitude active sleep-specific IPSPs.

261 potentials (APs) in a manner that suggested IPSPs enhanced postsynaptic Nav channel availability.

262 ocker picrotoxin, whereas the slow sustained IPSPs were blocked by the GABAB receptor blocker CGP-546

263 Carbenoxolone abolished all synchronized IPSPs in CA3 cells elicited by 4AP in the presence of io

264 (Nav) channels actively truncated synthetic IPSPs and were required for autonomous activity.

265 , confirming that in our experimental system IPSPs were both necessary and sufficient for synchrony.

266 These data indicate that IPSPs with reversal potentials positive to spike thresho

267 of the recorded EPSPs and IPSPs reveal that IPSPs are important in controlling the timing and probab

268 The IPSP had a reversal potential near -70 mV and was blocke

269 The IPSP HW was 13.4 +/- 2.8 ms in fast-spiking (n = 16) and

270 0.03) and a positive correlation between the IPSP conductance and PCr/ATP (P < 0.05).

271 M) (253 +/- 74 % of control) and blocked the IPSP(B) that preceded it.

272 On activation by the IPSP, I(H) potently accelerates the membrane time consta

273 st [Nphe1]-nociceptin(1-13)NH2 increased the IPSP amplitudes in restraint rats but not in unrestraint

274 mu-opioid receptor activation inhibited the IPSP at all concentrations and increased the maximal inh

275 produce an increase in the amplitude of the IPSP in the A photoreceptor in response to an evoked spi

276 Suppression of the IPSP resulted from presynaptic inhibition of the release

277 1 (10 microM) increased the amplitude of the IPSP(B) by 141 +/- 38 % and depressed the amplitude of t

278 occupancy and increased the amplitude of the IPSP.

279 not demonstrated until recently, because the IPSPs recorded at the soma are surprisingly small.

280 G-protein mediation of the IPSPs was ruled out using guanosine 5'-O-(2-thiodiphosph

281 (1) the number of independent sources of the IPSPs; (2) the rate at which each source was bombarded w

282 However, the GluR5 agonist ATPA reduced the IPSPs originating from the thalamic reticular nucleus.

283 tributions of these different factors to the IPSPs produced by two kinetically and anatomically disti

284 e modulator zolpidem strongly enhanced these IPSPs (45 +/- 28 %, n = 5).

285 ct on the other waveform parameters of these IPSPs (e.g., latency-to-onset, latency-to-peak, duration

286 tudy was directed to determine whether these IPSPs, that are specific to the state of active sleep, a

287 es by which thalamic relay neurons translate IPSPs into suprathreshold output and demonstrate extrath

288 The oscillatory mechanisms underlying IPSP-triggered LTSs crowned by spike bursts were investi

289 ion of large chloride driving force, unitary IPSP summation, and incomplete synaptic depression.

290 Notably, kinetics of dendritic unitary IPSPs were as fast as kinetics of somatic unitary IPSPs.

291 were as fast as kinetics of somatic unitary IPSPs.

292 Here, we show that unitary IPSPs (uIPSPs) modulate gain and unitary EPSP (uEPSP)-ac

293 ts and recorded, for the first time, unitary IPSPs from a GP-GP GABAergic connection.

294 When IPSPs replace the hyperpolarizing step in the induction

295 of firing was reduced but still evident when IPSPs were prevented by GABA(A) receptor antagonists.

296 P-AP coupling was dramatically improved when IPSPs preceded EPSPs.

297 S shape with a linear central portion where IPSP amplitude is between -0.2 and -0.6 as large as spik

298 e shunting even at high frequencies at which IPSPs sum.

299 o-olivary firing rates varied inversely with IPSP frequency, and the timing of Purkinje IPSPs and nuc

300 cells, outputs from IB cells associated with IPSPs, whereas those from layer 5 RS neurons related to