ライフサイエンスコーパス: EPSC

1 EPSC waveforms consisted of multiple peaks, probably res

2 EPSCs activated at proximal and distal dendritic locatio

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

4 EPSCs had enriched molecular signatures of blastomeres a

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

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

7 tex pyramidal neurons without affecting AMPA EPSC currents.

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

9 tors akin to that of slow NMDA and fast AMPA EPSCs at glutamate synapses.

10 ly by increased rectification ratio of AMPAR EPSCs and elevated early-phase long term potentiation (L

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

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

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

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

15 Though KO CFs evoked larger amplitude EPSCs, the charge transfer was the same as wild-type as

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

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

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

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

20 rating mammalian pluripotent stem cells, and EPSCs present a unique cellular platform for translation

21 presynaptic membrane capacitance changes and EPSCs.

22 s received similar numbers of inhibitory and EPSCs.

23 esting that the relative timing of IPSCs and EPSCs may permit excitation to drive additional eurydend

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

25 through the timing and strength of IPSCs and EPSCs, produces sparse and reliably timed cortical neuro

26 had basal firing rates near 8 spikes/s, and EPSCs and IPSCs were evident.

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

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

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

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

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

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

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

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

35 nchronous ST-EPSCs and trailing asynchronous EPSCs.

36 ing cue re-exposure significantly attenuated EPSC amplitude at T-LA synapses, suggesting that CaN aff

37 Binaural EPSCs often showed a nonlinearity that strengthened the

38 Both EPSCs and IPSCs have slow kinetics in prehearing animals

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

40 taminase (PG) on evening primrose seed cake (EPSC) protein and its effect on structure (amino acid co

41 odel, whereby expanded-potential stem cells (EPSC)-derived microglia-like cells are conditioned by sy

42 derived mouse expanded potential stem cells (EPSCs) from individual blastomeres by inhibiting the cri

43 hich we named expanded-potential stem cells (EPSCs).

44 tured under extended pluripotent conditions (EPSCs) can be partnered with trophoblast stem cells to s

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

46 In contrast, EPSCs were reduced in CA1 neurons neighboring ephrin-B1-

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

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

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

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

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

52 1-mediated excitatory postsynaptic currents (EPSCs) and associated calcium transients are increased a

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

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

55 classical excitatory postsynaptic currents (EPSCs) are followed by GABA(A) receptor-independent outw

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

57 mapping of excitatory postsynaptic currents (EPSCs) in L2/3 shows that the relative excitation of par

58 ibition of excitatory postsynaptic currents (EPSCs) in NAcSh principal medium spiny neurons (MSNs).

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

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

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

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

63 nje neuron excitatory postsynaptic currents (EPSCs).

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

65 nsmission (excitatory postsynaptic currents, EPSCs).

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

67 transmission to Bergmann glia and decreased EPSC decay time.

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

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

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

71 It takes 2-3 weeks to derive EPSCs from each cell source.

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

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

74 by PG have great potential to produce edible EPSC protein with modified techno-functional characteris

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

76 led protocols that describe how to establish EPSCs from single eight-cell-stage blastomeres or whole

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

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

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

80 her complex reduced neuron growth and evoked EPSCs (eEPSCs), however, the effects of mTORC1 on eEPSCs

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

82 ptogenetic excitation of vGluT2 cells evoked EPSCs in neighbouring neurons, indicating local synaptic

83 ased amplitude and faster decay of CF-evoked EPSCs.

84 Nitric oxide (NO) donors evoked EPSCs in T-stellate cells but not in the other types of

85 ic release properties of electrically-evoked EPSCs, suggesting a postsynaptic mechanism.

86 ntal coactivation, presynaptic firing evoked EPSCs of uniform amplitude whose frequency depended on t

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

88 roups: frequency/amplitude of mEPSCs, evoked EPSCs, paired pulse plasticity, rundown kinetics upon in

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

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

91 mediated mEPSCs and the amplitudes of evoked EPSCs and puff NMDAR currents in spinal dorsal horn neur

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

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

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

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

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

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

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

99 er synchronization index than smaller evoked EPSCs.

100 2 increases the amplitude of uncaging-evoked EPSCs (2pEPSCs) and calcium transients (2pCaTs) at a sub

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

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

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

104 Together, the larger, faster EPSCs in the KO explain the altered complex spike respon

105 d expression of GluA3 and GluA4 subunits for EPSCs.

106 de TS and XEN cell lines can be derived from EPSCs in vitro.

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

108 anced short-term depression of glutamatergic EPSCs.

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

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

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

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

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

114 nal modeling demonstrated that the increased EPSC amplitude can be partly attributed to the more prox

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

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

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

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

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

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

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

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

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

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

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

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

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

128 Large EPSCs therefore enhance the precision of spike timing.

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

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

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

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

133 This is the fastest NMDAR-mediated EPSC reported.

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

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

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

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

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

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

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

141 tic spine density and AMPA-receptor-mediated EPSCs in wild-type neurons, but not in Nlgn1 knock-out n

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

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

144 xybenzoic acid (3Cl-HBA) decreased miniature EPSC frequency, increased paired-pulse ratio, decreased

145 was accompanied by a reduction in miniature EPSC (mEPSC) frequency (but not mIPSC frequency), indica

146 e (~2 d) and involved decreases in miniature EPSC amplitude.

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

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

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

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

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

152 ocked PCB 95 effects on spines and miniature EPSCs.

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

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

155 r PSD95 protein levels, and larger miniature EPSCs.

156 tatic regulation of AMPAR-mediated miniature EPSCs in layer 2/3 of visual cortex.

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

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

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

160 atic increase in the amplitudes of miniature EPSCs (mEPSCs).

161 nduces an increase of frequency of miniature EPSCs and a decrease of paired pulse facilitation, assoc

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

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

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

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

166 oth the frequency and amplitude of miniature EPSCs.

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

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

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

170 of mEPSCs and the amplitudes of monosynaptic EPSCs evoked from the dorsal root and puff NMDAR current

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

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

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

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

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

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

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

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

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

180 24 hr) firing depressed both AMPAR and NMDAR EPSCs and eliminated spines, indicative of a synapse eli

181 density, and enhanced evoked AMPAR and NMDAR EPSCs.

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

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

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

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

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

187 abolishes the developmental change in NMDAR-EPSC decay time.

188 ated excitatory postsynaptic currents (NMDAR-EPSCs) during early life, whereas deletion of both Grin2

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

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

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

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

193 not affected, the postsynaptic LTP of NMDAR-EPSCs was reduced.

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

198 lity, emulsifying and foaming properties) of EPSC protein were evaluated.

199 Using the rate of EPSC block by IEM-1460, an open channel blocker of Ca(2+

200 By quantifying the rate of EPSC block by IEM-1460, we found an increased heterogene

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

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

203 a higher potency than the NMDAR component of EPSCs.

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

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

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

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

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

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

210 al calcium currents but reduced frequency of EPSCs.

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

212 enced by reduced zinc-mediated inhibition of EPSCs.

213 nced by enhanced zinc-mediated inhibition of EPSCs.

214 ck on itself by enhancing the probability of EPSCs.

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

216 as significantly correlated with the size of EPSCs.

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

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

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

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

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

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

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

224 can be generated from both human and porcine EPSCs.

225 Here, we report the derivation of porcine EPSCs, which express key pluripotency genes, are genetic

226 functional attributes reminiscent of porcine EPSCs.

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

228 ng late postnatal development, we quantified EPSCs and calcium entry in MSO neurons of Mongolian gerb

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

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

231 led to a reduction in synaptic NMDA-receptor EPSCs, without changing the subunit composition or the p

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 We recorded EPSCs from CA1 pyramidal cells in hippocampal slices fro

235 tagamma subunits directly into cones reduced EPSC amplitude.

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

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

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

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

240 l fibers expressing ChR2 demonstrated robust EPSCs in ipsilateral granule cells and enhanced the effe

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

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

243 Similar EPSC reduction occurred when PMCA activation was prevent

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

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

246 emory reconsolidation-associated spontaneous EPSC (sEPSC) frequency in BLA principal neurons during m

247 n Ca(2+) current likely enhanced spontaneous EPSC frequencies.

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

249 ike firing due to an increase in spontaneous EPSC frequencies.

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

251 GE-derived interneurons, reduces spontaneous EPSC frequency coupled to a reduction in dendritic gluta

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

253 depolarized neurons and enhanced spontaneous EPSCs.

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

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

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

257 al cells significantly more than spontaneous EPSCs.

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

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

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

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

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

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

264 or TH neurons augments IPSCs and suppresses EPSCs in Chx10 neurons by activating postsynaptic D(2) r

265 During swimming, EPSC and IPSC rates increased.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

280 The EPSCs derived from these protocols can differentiate int

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

282 onsequently, presynaptic Na(+) increased the EPSCs and was required to maintain the reliable high-fre

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

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

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

286 , or somatic cells directly reprogrammed, to EPSCs that display the molecular and functional attribut

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

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

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

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

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

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

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

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

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

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

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

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

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.