ライフサイエンスコーパス: EPSC

1 EPSC potentiation and attenuation were mediated by CRF-R

2 EPSC waveforms consisted of multiple peaks, probably res

3 EPSCs activated at proximal and distal dendritic locatio

4 EPSCs and IPSCs were well correlated except in center-pr

5 EPSCs in the STN were mediated primarily by AMPA and NMD

6 EPSCs were eliminated by tetrodotoxin, reinstated by 4-a

7 EPSCs were evoked by paired-pulse stimulation or by appl

8 Altering EPSC size with dynamic clamp, we found that a larger-tha

9 tex pyramidal neurons without affecting AMPA EPSC currents.

10 LTP of NMDA and AMPA EPSCs after high-frequency stimulation was reduced by pr

11 permeable AMPARs with Naspm reduced the AMPA EPSCs in IL neurons to a larger degree after extinction.

12 ot alter leptin-induced suppression of AMPAR EPSCs.

13 that 1 week later the AMPA receptor (AMPAR)-EPSC decay was slowed and mRNA for GluA1 increased while

14 Acoustic trauma (AT, loud sounds) slow AMPAR-EPSC decay times, increasing GluA1 and decreasing GluA4

15 ated excitatory postsynaptic currents (AMPAR-EPSCs), enhanced depression of AMPAR-EPSCs by NASPM (a s

16 (AMPAR-EPSCs), enhanced depression of AMPAR-EPSCs by NASPM (a selective CP-AMPAR antagonist), and in

17 amidal neurons, and also had higher IPSC and EPSC frequencies than adapting neurons.

18 ction of AT at around P20 disrupted IPSC and EPSC integration in the LSO, so that 1 week later the AM

19 al modelling confirmed that matched IPSC and EPSC kinetics are required to generate mature interaural

20 valbumin-positive cells evoked full SWRs and EPSC sequences in pyramidal cells.

21 presynaptic membrane capacitance changes and EPSCs.

22 s received similar numbers of inhibitory and EPSCs.

23 IPSCs and EPSCs show rapid acceleration during development, so tha

24 rvation was a reduced frequency of IPSCs and EPSCs, whereas the amplitudes were not modified.

25 operties and modulation of DA transients and EPSCs measured using fast-scan cyclic voltammetry and wh

26 DA transients and EPSCs were inhibited by DA receptor D2R agonist and show

27 amine were complex: ketamine enhanced apical EPSC responses in all mPFC subregions, anterior cingulat

28 ally low-pass filtered, resonance emerged as EPSC amplitude increased.

29 ocations, which likely explains asynchronous EPSC peaks, and we observed broadening of the axonal spi

30 ith EGTA-AM or BAPTA-AM reduced asynchronous EPSC rates earlier and to a greater extent than synchron

31 Synchronous and asynchronous EPSCs evoked within approximately 100 ms of GABA uncagin

32 ly reduced both synchronous and asynchronous EPSCs without altering spontaneous or thermal-evoked tra

33 is characterized by substantial asynchronous EPSCs following action potential-synched EPSCs and high

34 nchronous ST-EPSCs and trailing asynchronous EPSCs.

35 Binaural EPSCs often showed a nonlinearity that strengthened the

36 Both EPSCs and IPSCs have slow kinetics in prehearing animals

37 ncy-dependent threshold for repetitive brief EPSC stimuli and preferred frequency for spiking calls f

38 e VGCCs with omega-agatoxin IVA also changes EPSC amplitude by reducing both p and the effective RRP

39 ion-evoked long-lasting polysynaptic complex EPSCs in SNr GABA neurons.

40 NAS-181 increased the STN-triggered complex EPSCs and burst firing in SNr GABA neurons, demonstratin

41 amplitude occlusion) in pairs of consecutive EPSCs due to receptor saturation.

42 ated by the back-extrapolation of cumulative EPSC amplitudes during a train of 30 action potentials a

43 and average excitatory postsynaptic current (EPSC) amplitude, were unaffected by noise rearing, sugge

44 ads to mean excitatory postsynaptic current (EPSC) amplitudes that are independent of Ca(2+) current.

45 ents, NMDAR excitatory postsynaptic current (EPSC) decay kinetics, progressive EPSC inhibition during

46 behaviors, excitatory post-synaptic current (EPSC), has been updated as a stretched-exponential funct

47 generating excitatory postsynaptic currents (EPSCs) and action potentials.

48 1-mediated excitatory postsynaptic currents (EPSCs) and associated calcium transients are increased a

49 R-mediated excitatory postsynaptic currents (EPSCs) and puff NMDA-elicited currents were recorded in

50 ls reduced excitatory postsynaptic currents (EPSCs) and spine density in mature neurons, whereas gene

51 pontaneous excitatory postsynaptic currents (EPSCs) during the symptomatic phase of EAE, suggesting a

52 eficits in excitatory postsynaptic currents (EPSCs) generated in apical dendritic spines of layer V p

53 Excitatory postsynaptic currents (EPSCs) in monosynaptic nTS neurons were recorded in the

54 on elicits excitatory postsynaptic currents (EPSCs) in NTS neurons mediated by both AMPA- and NMDA-ty

55 e examined excitatory postsynaptic currents (EPSCs) of dorsal horn neurons evoked by dorsal root stim

56 R-mediated excitatory postsynaptic currents (EPSCs) of dorsal horn neurons evoked by dorsal root stim

57 )-mediated excitatory postsynaptic currents (EPSCs) onto VTA dopamine neurons.

58 The excitatory postsynaptic currents (EPSCs) recorded in laminae III-V showed enhanced sensiti

59 luation of excitatory postsynaptic currents (EPSCs) revealed that rCASP6 rapidly increased synaptic t

60 Excitatory postsynaptic currents (EPSCs) were recorded from superficial dorsal horn neuron

61 nje neuron excitatory postsynaptic currents (EPSCs).

62 miniature excitatory postsynaptic currents (EPSCs).

63 S218L to study presynaptic Ca(2+) currents, EPSCs, and in vivo activity at the calyx of Held synapse

64 nsmission (excitatory postsynaptic currents, EPSCs).

65 d ectopic transmission to glia and decreased EPSC decay time with closely similar time courses.

66 transmission to Bergmann glia and decreased EPSC decay time.

67 ity-dependent long-term depression decreased EPSC decay time, revealing a 'late' current that is pres

68 r, the ability of CRF-R2 agonists to depress EPSCs and potentiate IPSCs was diminished.

69 Cocaine depressed EPSCs amplitude by 50% but enhanced the overall DA trans

70 and caused a larger reduction in cone-driven EPSCs ( approximately 30%).

71 activation-driven amplitude occlusion, each EPSC reduces amplitudes of subsequent events by an estim

72 a subset of mesolimbic DA neurons, eliciting EPSCs onto medium spiny neurons in NAc.

73 maximal transmission, and exhibited enhanced EPSC amplitude, charge, and RRP size compared to interne

74 itral cells have a prolonged afferent-evoked EPSC, which serves to amplify the synaptic input.

75 ke, which likely underlies changes to evoked EPSC onset.

76 ivation augmented solitary tract (TS) evoked EPSC amplitude whereas 5-HT2AR blockade depressed TS-EPS

77 Additionally, evoked EPSCs in afferent fibers are unaffected by glutamate tra

78 n unexpected finding: large-amplitude evoked EPSCs have a significantly larger synchronization index

79 -Astrocyte autaptic evoked EPSCs, but not IPSCs, displayed an altered temporal prof

80 om postnatal day (P)12-14 mice, light-evoked EPSCs were large (> 1 nA at -70 mV).

81 osure occluded AP5 inhibition of mPFC-evoked EPSCs, suggesting that D-serine reduced EPSCs by inhibit

82 strongly potentiated the amplitude of evoked EPSCs (eEPSCs), and reduced the EPSC paired-pulse ratio.

83 ts similarly reduced the amplitude of evoked EPSCs and the frequency of miniature EPSCs in dorsal hor

84 amplitude of mEPSCs and amplitudes of evoked EPSCs are unaltered.

85 Bayesian Quantal Analysis (BQA) of evoked EPSCs showed that the number of functional contacts on a

86 sm normalized the I-O relationship of evoked EPSCs, frequency of spontaneous EPSCs, and probability o

87 nd increased the NMDAR:AMPAR ratio of evoked EPSCs.

88 , oxotremorine-M failed to potentiate evoked EPSCs, and its inhibitory effect was abolished by himbac

89 evertheless significantly potentiated evoked EPSCs in a subpopulation of amacrine cells.

90 er synchronization index than smaller evoked EPSCs.

91 2 increases the amplitude of uncaging-evoked EPSCs (2pEPSCs) and calcium transients (2pCaTs) at a sub

92 on of inferior olivary axons in vitro evokes EPSCs in CbN cells of several hundred pA to more than 1

93 Interestingly, for spike-evoking EPSC trains, the threshold amplitude at spike resonant f

94 e was observed during trains of facilitating EPSCs recorded in 1.2 mM external Ca(2+) ([Ca(2+)]e).

95 half of the local GrC contacts generate fast EPSCs, indicating their basolateral location in the GL.

96 d expression of GluA3 and GluA4 subunits for EPSCs.

97 ocalized with CGRP, and activation generated EPSCs in dorsal anterolateral BNST neurons that elicited

98 anced short-term depression of glutamatergic EPSCs.

99 mice, photostimulation evoked an increase in EPSC frequency, whereas in P9-P15 mice the response swit

100 mice the response switched to a reduction in EPSC frequency, indicating a developmental excitatory-to

101 eptors prevented both the CRF-R2 increase in EPSCs and the attenuation produced by 1,3-dipropyl-8-cyc

102 concentration of EGTA led to a reduction in EPSCs that was significantly stronger in Munc13-3(-/-).

103 dendritic spine loss from P21, and increased EPSC frequency from P21 in SOD1 LVPNs.

104 nsity difference suggests that the increased EPSC duration after AT shifts interaural level differenc

105 CRF-R2 activation increased EPSCs as a result of a reduction of tonic GABA-dependent

106 r neurons ( approximately 26%) and increased EPSCs in significantly more neurons (33%) compared with

107 ctivated microglial culture medium increased EPSCs in spinal cord slices via TNF-alpha.

108 s genetic ablation of neurogenesis increased EPSCs in mature neurons.

109 eloping and mature dentate neurons increased EPSCs and prevented neurogenesis-induced synaptic suppre

110 stress did not induce a loss of CRF-induced EPSCs in basal dendrites, thereby creating a relative im

111 nd infralimbic (IL) but enhanced CRF-induced EPSCs only in AC and PL-responses were unchanged in IL,

112 plex 1 synaptogenic pathway; the CRF-induced EPSCs required an intact BLA input and were generated pr

113 Here we found that CRF induces EPSCs in PFC layer V cells and that ketamine enhanced th

114 In addition, D-serine inhibited EPSCs evoked at -70 mV in vitro by optogenetic stimulati

115 ent dendritic sites: one, with large initial EPSC amplitude, saturated after three stimuli and domina

116 re step sequence can be predicted from input EPSCs and output spikes of a single granule cell, sugges

117 Large EPSCs therefore enhance the precision of spike timing.

118 ed; PV neurons received significantly larger EPSCs compared with SOM neurons, and the degree of phase

119 ifference functions, and that longer-lasting EPSCs compensate to maintain binaural function with rais

120 n sustained increases in amplitudes of later EPSCs during trains of 10 stimuli at 10-20 Hz.

121 ot ganglia (DRG) neurons and on miniature (m)EPSCs recorded from large lamina I neurons in horizontal

122 This is the fastest NMDAR-mediated EPSC reported.

123 EtOH (66 mM) had no effect on AMPA-mediated EPSCs but decreased those mediated by NMDA receptors.

124 AMPA-mediated EPSCs showed an unusually wide range of decay time const

125 The rapid appearance of AMPAR-mediated EPSCs and the lack of maturational changes show that GAB

126 ll synapse in the cerebellum, AMPAR-mediated EPSCs last for hundreds of milliseconds, and it has been

127 pulse ratio of EPSCs, smaller AMPAR-mediated EPSCs, smaller AMPA currents, greater NMDAR-mediated EPS

128 hort-term plasticity of mossy fibre-mediated EPSCs.

129 it resulted in detectable glutamate-mediated EPSCs as well as GABA-mediated IPSCs, although the net e

130 tes Nts1, thereby potentiating NMDA-mediated EPSCs and promoting reward.

131 (AMPAR) - and NMDA receptor (NMDAR)-mediated EPSCs and glycinergic IPSCs.

132 o of AMPAR-to-NMDA receptor (NMDAR)-mediated EPSCs.

133 NMDAR-mediated EPSCs and puff NMDA-elicited currents were recorded in s

134 trations 24(S)-HC potentiates NMDAR-mediated EPSCs in rat hippocampal neurons but fails to affect AMP

135 maller AMPA currents, greater NMDAR-mediated EPSCs, greater NMDA currents, lower AMPAR-mediated/NMDAR

136 AMPA and NMDA receptor-mediated EPSCs were equally inhibited by cocaine, suggesting a pr

137 resting levels while in wildtype PNs mGluR1 EPSCs are enhanced by elevated [Ca(2+)].

138 sion accompanied by an increase in miniature EPSC amplitudes and rise times.

139 ysiological analysis of changes in miniature EPSC and IPSC properties in L2 pyramidal neurons showed

140 c activity revealed an increase in miniature EPSC frequency restricted to aged animals with preserved

141 ed pulse facilitation and increase miniature EPSC frequency without a change in amplitude.

142 ynapses as determined by increased miniature EPSC (mEPSC) frequency without changes in presynaptic pa

143 eficient neurons exhibit increased miniature EPSC amplitudes, and their remaining spines exhibit larg

144 ransporters with MeAIB reduced the miniature EPSC amplitude significantly.

145 ize and compactness in parallel to miniature EPSC amplitude.

146 ncreased spine density and altered miniature EPSCs, confirming a physiological involvement of caspase

147 ntials (EPSPs) and spontaneous and miniature EPSCs (s/mEPSCs) by mainly decreasing glutamate release

148 The frequency of spontaneous and miniature EPSCs in most dorsal horn neurons was profoundly increas

149 out (4E-BP2(-/-)) mice, evoked and miniature EPSCs were increased, an effect mimicked by short-hairpi

150 ocked PCB 95 effects on spines and miniature EPSCs.

151 ive (action potential-independent) miniature EPSCs exhibited significantly higher frequency, greater

152 the frequency of capsaicin-induced miniature EPSCs in the presence of tetrodotoxin and omega-conotoxi

153 r PSD95 protein levels, and larger miniature EPSCs.

154 ly released glutamate, we measured miniature EPSCs to assess vesicular glutamate content.

155 higher frequency of NMDAR-mediated miniature EPSCs of PVN neurons in SHRs.

156 plitude of spontaneously occurring miniature EPSCs (mEPSCs) was reduced in neurons from stg/stg mice,

157 Voltage-clamp recordings of miniature EPSCs (mEPSCs) from NST neurons show that astrocytes con

158 and the amplitude and frequency of miniature EPSCs in Abeta-treated neurons, whereas upregulation of

159 evoked EPSCs and the frequency of miniature EPSCs in dorsal horn neurons of FK506-treated rats.

160 spine density and the frequency of miniature EPSCs in primary dissociated rat hippocampal cultures co

161 at exhibit increased amplitudes of miniature EPSCs indicative of excessive postsynaptic excitation.

162 plitude and decreased frequency of miniature EPSCs induced by Rich2 overexpression, while si-RNA trea

163 Kinetic analysis of miniature EPSCs revealed quantal release of mixed events associati

164 frequency but not the amplitude of miniature EPSCs, suggesting a reduced vesicular release.

165 oth the frequency and amplitude of miniature EPSCs.

166 ndicated by increased frequency of miniature EPSCs.

167 latency, less frequent and smaller miniature EPSCs, higher paired-pulse ratio of EPSCs, smaller AMPAR

168 se in the frequency of spontaneous miniature EPSCs and interestingly, miniature IPSCs.

169 The miniature EPSCs in Nrg1 heterozygous animals have a faster time co

170 Endocannabinoids did not tonically modify EPSCs.

171 Summation of the monaural EPSCs predicted the binaural excitatory response but les

172 mice, oxotremorine-M inhibited monosynaptic EPSCs in significantly fewer neurons ( approximately 26%

173 ne-M decreased the amplitude of monosynaptic EPSCs in approximately 67% of neurons but increased it i

174 iting the voltage dependence of monosynaptic EPSCs similarly indicated dominant expression of GluN2A/

175 However, summation of N1/N2B and N1/N2A EPSCs could not account for the deactivation kinetics of

176 used modest suppression of monosynaptic NMDA EPSC amplitudes, but had a widely variable, sometimes po

177 al network resulted in an inhibition of NMDA EPSC potentiation that was rescued by adding extracellul

178 annel activity reduced the amplitude of NMDA EPSCs in mouse layer 5 prefrontal cortex pyramidal neuro

179 This reduction of NMDA EPSCs was rescued by addition of D-serine in the extrace

180 al network resulted in the reduction of NMDA EPSCs, which was rescued by adding extracellular D-serin

181 y more important roles for polysynaptic NMDA EPSCs driven by primary afferents following disinhibitio

182 cked both monosynaptic and polysynaptic NMDA EPSCs initiated by primary afferent activation by approx

183 at GluN2D does not detectably slow the NMDAR EPSC time course at this age.

184 24 hr) firing depressed both AMPAR and NMDAR EPSCs and eliminated spines, indicative of a synapse eli

185 XCAR similarly curtailed NMDAR EPSCs of minimal amplitude, but had no effect on small A

186 Furthermore, the decay kinetics of NMDAR EPSCs was significantly prolonged, suggesting insertion

187 In mouse hippocampal slices, NMDAR EPSCs in a singly activated CA1 pyramidal neuron were re

188 The NMDA receptor (NMDAR)-EPSC decay tau accelerated from >40 ms in prehearing ani

189 In contrast, GlyR IPSC and NMDAR-EPSC decay times were unchanged.

190 The basal amplitude of evoked NMDAR-EPSCs and puff NMDA currents in retrogradely labeled PVN

191 The basal amplitudes of evoked NMDAR-EPSCs and puff NMDA currents were significantly higher i

192 normalized the increased amplitude of NMDAR-EPSCs and puff NMDA currents in labeled PVN neurons in S

193 gnificantly increased the amplitude of NMDAR-EPSCs and puff NMDA currents in PVN neurons in WKY rats

194 The NMDAR-EPSCs accelerate over development to achieve decay time-

195 ic clamp, we found that a larger-than-normal EPSC increased information flow through the synapse.

196 0, reverses the increase in the amplitude of EPSC(A).

197 uced the CB1 receptor-mediated inhibition of EPSC and the eCB-mediated depolarization-induced suppres

198 there was no activity-dependent mGlu1-LTD of EPSC(NMDA) at the TA-CA1 pathway, or effects on subseque

199 easuring the paired-pulse ratio, variance of EPSC amplitudes, and response probability.

200 ei associated with the reduced amplitudes of EPSCs evoked by AN stimulation.

201 ts contributed to the enhanced amplitudes of EPSCs evoked by input from the primary afferents in neur

202 a higher potency than the NMDAR component of EPSCs.

203 Decay time constants of EPSCs increased (or decreased) in the presence of a glut

204 s prediction by measuring the time course of EPSCs in ON-type SBACs in the mouse retina, activated by

205 trolled the slow deactivation time course of EPSCs in the STN.

206 than GABAA receptor-mediated enhancement of EPSCs, suggesting GABAB receptors may be selectively act

207 Examination of EPSCs revealed the targeting of gamma-2 to be synapse-sp

208 onitoring the alteration in the frequency of EPSCs during photostimulation of interneurons.

209 al calcium currents but reduced frequency of EPSCs.

210 prevented the cocaine-induced inhibition of EPSCs and caused a larger increase in DA transient peak,

211 tude and increased the paired-pulse ratio of EPSCs evoked by electrical stimulation in slices from co

212 iniature EPSCs, higher paired-pulse ratio of EPSCs, smaller AMPAR-mediated EPSCs, smaller AMPA curren

213 Using whole-cell patch-clamp recordings of EPSCs in nucleus accumbens, we demonstrated that gabapen

214 get neurons, and slowed-down the recovery of EPSCs after depleting stimuli.

215 i, consistent with unaltered I-V relation of EPSCs mediated by GluA1/GluA2 heteromers.

216 as significantly correlated with the size of EPSCs.

217 Trains of EPSCs (5 Hz) depressed strongly throughout development,

218 ugmentation in quantal size during trains of EPSCs, and application of the low-affinity glutamate rec

219 pared from MKP-2(-/-) mice with no effect on EPSC amplitude observed.

220 caging of RuBi-GABA has a biphasic effect on EPSC amplitudes recorded from stellate cells.

221 that synaptic plasticity has no influence on EPSC amplitude or spiking.

222 nd potentiating effects of oxotremorine-M on EPSCs in M3 single-KO and M1/M3 double-KO mice were simi

223 rnal tufted cells had a 4.1-fold larger peak EPSC amplitude, integration of the evoked currents showe

224 probability, suggesting that the larger peak EPSC in external tufted cells was the result of more syn

225 tic capacitance changes and the postsynaptic EPSC at rat calyx of Held synapses in the absence or pre

226 -rising excitatory post-synaptic potentials (EPSCs) to the model.

227 Monaural stimulation in either ear produced EPSCs and IPSCs in most neurons.

228 in DbetaH(Cre/0) mouse brain slices produced EPSCs in 71% of tested DMV preganglionic neurons (PGNs)

229 c current (EPSC) decay kinetics, progressive EPSC inhibition during repetitive stimulation, and extra

230 to CbN cells generate unitary AMPA receptor EPSCs of approximately 1 nS that decay in approximately

231 s and mildly voltage-dependent NMDA receptor EPSCs of approximately 0.6 nS that decay in approximatel

232 Comparison with intracellularly recorded EPSCs revealed that most properties of ANF spike trains

233 We recorded EPSCs and IPSCs to examine the buildup of neuronal activ

234 tagamma subunits directly into cones reduced EPSC amplitude.

235 oked EPSCs, suggesting that D-serine reduced EPSCs by inhibiting HA-NMDARs.

236 hat photostimulation of interneurons reduces EPSC frequency at ages P3-P9.

237 rallel fibers and deconvolution of resulting EPSCs using quantal signals as template.

238 Whole-cell recordings reveal EPSCs following stimulation of VTA glutamate terminals i

239 Thus, the evolutionarily selected EPSC size does not maximize retinal information flow to

240 -evoked (eEPSCs) and/or spontaneous (sEPSCs) EPSCs at solitary tract nucleus neurons.

241 Similar EPSC reduction occurred when PMCA activation was prevent

242 arance of synaptic glutamate during the slow EPSC is dictated by an uptake process.

243 ts 3 and 10 days after SNL displayed smaller EPSCs with prolonged latency, less frequent and smaller

244 Purkinje cells suggests that the brief spine EPSCs cause the activated T-type channels to deactivate

245 Furthermore, spontaneous EPSC (sEPSC) frequency was increased in acute slices and

246 -induced allodynia and increased spontaneous EPSC (sEPSC) frequency by suppressing RIM1alpha-facilita

247 t (IL-1ra) in EAE slices reduced spontaneous EPSC alterations.

248 BOA, both the near threshold and spontaneous EPSCs contained a significant CI-AMPAR component.

249 depolarized neurons and enhanced spontaneous EPSCs.

250 g2576 DG granule cells exhibited spontaneous EPSCs that were higher in frequency but not amplitude co

251 ptin diminished the frequency of spontaneous EPSCs onto OX neurons.

252 at CRF enhances the frequency of spontaneous EPSCs onto VTA-projecting BNST neurons in naive mice.

253 ip of evoked EPSCs, frequency of spontaneous EPSCs, and probability of release that, in turn, correla

254 ainly inhibitory GABA actions on spontaneous EPSCs in the immature hippocampus and neocortex in vivo

255 al cells significantly more than spontaneous EPSCs.

256 Previously, we have shown that spontaneous EPSCs differed markedly in layer 3 pyramidal neurons of

257 As with spontaneous EPSCs, TTX-insensitive (action potential-independent) mi

258 and to a greater extent than synchronous ST-EPSC amplitudes without altering sEPSCs or thermal sensi

259 trast, their relative contribution to the ST-EPSC is much less during low (<2 Hz) frequency stimulati

260 solitary tract (ST) triggered synchronous ST-EPSCs and trailing asynchronous EPSCs.

261 While weak subthreshold EPSC trains were essentially low-pass filtered, resonanc

262 ous EPSCs following action potential-synched EPSCs and high spontaneous rates that are thermally sens

263 TC EPSCs on FS neurons were larger and showed steeper short

264 ASIC1a decreased spontaneous IPSCs more than EPSCs, and increased the excitability of the BLA network

265 ept for one skipped stimulus, and found that EPSC amplitude was affected for 60 ms following a skippe

266 ng to identify synaptic inputs, we show that EPSCs from aa and mf contacts in basolateral dendrites d

267 Two months after AT the EPSC decay times recovered to control values.

268 ction potentials, we show that, instead, the EPSC size optimizes the ratio of retinal information tra

269 ithout inhibiting the NMDAR component of the EPSC and shows neuroprotective activity in vivo without

270 Purkinje cells indicate that phase 1 of the EPSC arises from synapses ideally suited to transmit sho

271 onist, we describe a T-type component of the EPSC that is activated by the AMPA receptor-mediated dep

272 Using current voltage analysis of the EPSC we show that light intensities near RGC threshold,

273 This component can amount up to 20% of the EPSC, and this fraction is maintained even at the high f

274 de of evoked EPSCs (eEPSCs), and reduced the EPSC paired-pulse ratio.

275 s the AMPAR subunits expressed and slows the EPSC time-course at synapses in the central auditory sys

276 block, which was highly correlated with the EPSC amplitude (or the amount of glutamate release).

277 The EPSCs are multipeaked, owing to burst firing in several

278 The EPSCs had three patterns in response to ABL stimuli, pre

279 g of the spikes was sharper than that of the EPSCs.

280 The amplitude of these EPSCs decreased over development, reaching a plateau of

281 Thus, EPSCs should be small to minimize energy use, but not so

282 In control tissue, EPSCs displayed concentration-dependent, bimodal respons

283 The PF train EPSC consisted of two components that were present in va

284 li and dominated the late phase of the train EPSC.

285 i and dominated the early phase of the train EPSC; and the other, with small initial amplitude, incre

286 Analysis of train EPSCs revealed two synaptic components, phase 1 and 2.

287 (mGlu1-LTD) of NMDAR-mediated transmission (EPSC(NMDA)) at the SC-CA1 input prevents subsequent LTP

288 MPA receptor-mediated synaptic transmission (EPSC(A)) when applied intracellularly.

289 e solitary tract (ST) always (93%) triggered EPSCs at CeA projecting NTS neurons.

290 ed to stratum lacunosum-moleculare triggered EPSCs both on local interneurons and on pyramidal cells.

291 litude whereas 5-HT2AR blockade depressed TS-EPSC amplitude at low and high TS stimulation rates.

292 es of NMDA receptors contribute to wild-type EPSCs, with at least two-thirds being triheteromeric rec

293 t for the deactivation kinetics of wild-type EPSCs.

294 time, and decay time constant of the unitary EPSC were not different for L2/3-->corticocollicular and

295 Unitary EPSCs recorded from Munc13-3(-/-) GCs showed normal kine

296 Unitary EPSCs were small and brief (AMPA receptor, approximately

297 However, short trains of unitary EPSCs showed no synaptic depression in L2/3-->corticocol

298 lly, translation-dependent cL-LTP of unitary EPSCs was also affected in 4E-BP2(-/-) mice, lowering in

299 00 ms of GABA uncaging were increased, while EPSCs evoked approximately 300-600 ms after GABA uncagin

300 in the LSO matures by postnatal day 20, with EPSCs and IPSCs having fast kinetics.