ライフサイエンスコーパス: EPSP

1 s during excitatory postsynaptic potentials (EPSPs).

2 red with excitatory postsynaptic potentials (EPSPs).

3 uts, via excitatory postsynaptic potentials (EPSPs).

4 -enolpyruvyl-shikimate-3-phosphate synthase (EPSPs).

5 ecay of excitatory post-synaptic potentials (EPSPs).

6 large-amplitude, nondendrodendritic [LANDD] EPSPs).

7 of the isolated CI-AMPAR component of the MF EPSP.

8 not CX546, which differ in their effects on EPSPs.

9 rneurons, BFc inputs elicited fast nicotinic EPSPs.

10 mutation to create the highly resistant TIPS EPSPS.

11 gain by inhibiting summation of subthreshold EPSPs.

12 ve a target-site mutation at position 106 of EPSPS.

13 potentials or on the frequency of miniature EPSPs.

14 ntibody occluded the SNX-induced increase of EPSPs.

15 chips, and cornmeal for the presence of CP4 EPSPS.

16 r inhibitory and weak tonic-like "modulator" EPSPs.

17 related to nested bursts of theta-frequency EPSPs.

18 tion neurons were not able to inhibit evoked EPSPs.

19 cy, but not amplitude, of glutamatergic mini EPSPs.

20 ic corticospinal neurons had faster decaying EPSPs.

21 s result in the largest and sharpest somatic EPSPs.

22 coincidence of the rising slopes of unitary EPSPs.

23 3 to 18 mum, versus 9.5 mum for native maize EPSPS.

24 et firing was triggered by IPSPs rather than EPSPs.

25 induced neuroplasticity mimicking the LTP of EPSPs.

26 l or cortical stimulation with glutamatergic EPSPs.

27 e initiation and by subthreshold boosting of EPSPs.

28 se, EPSPS) and increased gene copy number of EPSPS.

29 n potentials evoked by single AMPA-dependent EPSPs.

30 een postsynaptic action potentials (APs) and EPSPs.

31 hrough comparisons of the relative timing of EPSPs.

32 amplification of integrated corticothalamic EPSPs.

33 initial excitatory postsynaptic potentials (EPSPs), a graded activation profile, and a metabotropic

34 We find that the amplitude of the EPSP abruptly increases during middle age and that this

35 levels also predicted the attenuation of the EPSP across the dendritic tree.

36 GCCs and A-type VGKCs are inactivated and CF-EPSPs activate P/Q-type VGCCs, high-voltage activated VG

37 el fiber excitatory postsynaptic potentials (EPSPs) activate Cav3 Ca(2+) influx to trigger a KCa3.1-m

38 zation associated with a climbing fiber (CF) EPSP activates voltage-gated Ca(2+) channels (VGCCs), vo

39 lls and, in contrast to its effect on SC-CA1 EPSPs, ADX71743 reversed the ability of high-frequency s

40 monosynaptic and only one weak oligosynaptic EPSP after stimulation of the ipsilateral corticospinal

41 sensitivity to the rate of depolarization by EPSPs, allowing neurons to assess the coincidence of the

42 EPSPs also could be amplified by the Na conductance when

43 (+) channels that suppresses NMDAR-dependent EPSP amplification at ventral SC synapses.

44 Computer simulations reveal that EPSP amplification by T-type Ca(2+)channels and NMDA rec

45 Consequently, postsynaptic EPSP amplification mechanisms limit the "modulatory" eff

46 Sst neuron firing was sufficient to enhance EPSP amplitude and reduce failure rates, effects that we

47 ting APs plays a key role in regulating both EPSP amplitude and STDP induction.

48 ng for dendritic attenuation and normalizing EPSP amplitude at the soma.

49 EPSP amplitude changes were correlated with changes of r

50 vation of mAChRs led to LTP, with changes in EPSP amplitude distributions consistent with a presynapt

51 Changes in EPSP amplitude distributions in dual recordings were con

52 ic patch recordings, we found that dendritic EPSP amplitude increased with distance from the soma, co

53 For 2/3 to 2/3 connections, mean EPSP amplitude was correlated with both Q and P(r) value

54 the nociceptin-induced inhibition of evoked EPSP amplitude was not significantly different from that

55 eurons from alpha(1A)(-)/(-) mice, while the EPSP amplitude was reduced by only 30% in CT mice.

56 x channels with Z941 reduce mitral-to-mitral EPSP amplitude, increase the coefficient of variation of

57 t affect ethanol-induced decreases in evoked EPSP amplitude.

58 ucing the excitatory postsynaptic potential (EPSP) amplitude through shunting.

59 Thr depletion in vitro increased both EPSP amplitudes and P-eIF2alpha.

60 rprisingly, we found no relationship between EPSP amplitudes and the similarity of RFs or responses,

61 pressed during spontaneous network activity: EPSP amplitudes are 2-fold smaller and failure rates are

62 lectrophysiological analyses show diminished EPSP amplitudes in monosynaptic sensory-motor circuits i

63 Local dendritic spontaneous EPSP amplitudes increased sharply in the dendrite with d

64 l (but not d)-threoninol also increased EPSP amplitudes relative to control.

65 hat latency shifts had only minor effects on EPSP amplitudes that were often <1.0 mV/ms shift.

66 In somatic recordings, EPSP amplitudes were largely uniform following minimal s

67 esponded to different stimuli with increased EPSP amplitudes.

68 ties (paired-pulse depression, large initial EPSPs, an all-or-none activation profile, and no metabot

69 es are observed in synaptic spines during an EPSP and back-propagating action potential due to the op

70 inhibition decreases the rising slope of the EPSP and prolongs the EPSP-to-AP transition time.

71 trigger a KCa3.1-mediated regulation of the EPSP and subsequent after-hyperpolarization.

72 able synaptic potentiation induced only when EPSPs and action potentials (APs) were paired within 8 m

73 otentiation arose from shunting of dendritic EPSPs and APs.

74 , suppressed stimulus-evoked purinergic slow EPSPs and ATP-induced slow EPSP-like response in guinea

75 NMDAR antagonists decreased EPSPs and EPSP-spike coupling more strongly in pyramidal

76 This short-circuits nearby EPSPs and is suggested here to contribute to the magnitu

77 is correlated with increased incidence of CF EPSPs and membrane depolarization.

78 Leptin also increased the size of evoked EPSPs and the ability of low-intensity solitary tract st

79 MDARs) activates spine SK channels, reducing EPSPs and the associated spine head Ca(2+) transient.

80 iven the tight association of single retinal EPSPs and the following inhibition, we propose that both

81 rease in EPSC duration increases the size of EPSPs and thereby markedly enhances the AP firing probab

82 tend to follow the timing of suprathreshold EPSPs and thus become less regular again.

83 We examined field EPSPs and whole-cell recordings in wild-type mouse hippo

84 comitant excitatory postsynaptic potentials (EPSPs) and dampens their temporal integration.

85 5-enolpyruvylshikimate-3-phosphate synthase, EPSPS) and increased gene copy number of EPSPS.

86 s both transgenic glyphosate resistance (CP4 EPSPS) and lepidopteran insect resistance (Cry1Ac).

87 mediated excitatory postsynaptic potentials (EPSPs) and spontaneous and miniature EPSCs (s/mEPSCs) by

88 de, increase the coefficient of variation of EPSPs, and increase paired-pulse ratios, consistent with

89 neurogliaform interneurons suppressed evoked EPSPs, and these effects were blocked by CGP 52432.

90 transiently increases the peak amplitude of EPSPs, and thus postsynaptic spiking probability.

91 timulation-triggered switch reduces both the EPSP-AP coupling and evoked AP doublets.

92 gered switch in GluR2 expression reduces the EPSP-AP coupling because of the decrease in the synaptic

93 ncorporation of GluR2 receptors enhances the EPSP-AP coupling, but the parallel fiber stimulation-tri

94 ion, measured as higher firing rate, shorter EPSP-AP delay in vivo and shorter AP latency in slice ex

95 measured as higher firing frequency, shorter EPSP-AP delay in vivo, and shorter AP latency in slice e

96 STDP disappeared with randomized EPSP/AP pairing or high intracellular Ca(2+) buffering,

97 layer may provide a reference for repetitive EPSP/AP phase coupling.

98 where on the head evoked large, monosynaptic EPSPs ( approximately 5-20 mV) in tINs, at mixed AMPAR/N

99 ing an IAA-deficient diet, the meal ends and EPSPs are activated in the APC; from there, neurons proj

100 Peak [Na(+)]i changes during single EPSPs are approximately 5 mm Stronger electrical stimula

101 trophysiological analysis further shows that EPSPs are decreased in these mice.

102 o understand how the timing and amplitude of EPSPs are maintained during propagation in the dendrites

103 orrelations demonstrate that fluctuations in EPSPs are significantly correlated to changes in postsyn

104 Excitatory postsynaptic potentials (EPSPs) are greatly prolonged, outlasting the neuronal me

105 RG diminished the contralateral motoneuronal EPSPs as well as a local injection of 6-cyano-7-nitroqui

106 onality of enolpyruvylshikimate 3-phosphate (EPSP) as a nonenzymatic analog of the EPSP synthase (Aro

107 1 of these 59 genes, with high expression of EPSPS, as well as genes coding for aminotransferases, zi

108 r data demonstrate that the amplitude of the EPSP at the Drosophila NMJ increases during aging and th

109 , these inputs produce a 5- to 6-fold larger EPSP at the soma of CA2 compared with CA1 PNs, which is

110 (m) and Ca(2+) transients associated with CF-EPSPs at different initial V (m), and we analyzed the ch

111 MSO neurons, the normalization of dendritic EPSPs at the soma would increase the importance of input

112 tic Ca(2+) and K(+) channels activated by CF-EPSPs, based on optical measurements of V (m) and Ca(2+)

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

114 tants of excitatory postsynaptic potentials (EPSPs), both increase along this axis.

115 Splanchnic F-EPSPs but not colonic F-EPSPs were reduced in CSE knock-

116 In contrast, EPSPs but not IPSPs were recorded after adding strychnin

117 LANDD EPSPs can be evoked by both focal stimulation near GC pr

118 5-Enolpyruvylshikimate-3-phosphate synthase (EPSPS) catalyzes the transfer of a carboxyvinyl group fr

119 with irreversible C3 protonation to form an EPSP cation intermediate; that is, an AH(double dagger)*

120 y is to stabilize the positive charge in the EPSP cation.

121 itory fast-spiking (FS) V1 cells had similar EPSP characteristics, showing that in the visual system,

122 ow here that iterative optimization of maize EPSPS containing the G101A substitution yielded variants

123 iginal optimization was conducted with maize EPSPS, contextually homologous substitutions conferred s

124 rbored an additional chromosome with several EPSPS copies besides the native chromosome pair with EPS

125 agreement with FISH results, segregation of EPSPS copies followed single-locus inheritance in GR1 po

126 llustrates the physical mapping of amplified EPSPS copies in A tuberculatus.

127 We analyzed the distribution of EPSPS copies in the genome of A tuberculatus using fluor

128 ed the genomic organization of the amplified EPSPS copies using fluorescence in situ hybridization (F

129 pies besides the native chromosome pair with EPSPS copies.

130 aster) subthreshold MPOs and slower (faster) EPSPs correlate with larger (smaller) grid spacings and

131 Notably, we found that slowed EPSP decay preferentially enhanced temporal summation an

132 and the lack of solvent hydron exchange into EPSP demonstrated that protonation was irreversible.

133 es not recover; however, electrically evoked EPSPs do recover.

134 sing inhibitory neurons received the largest EPSPs, dominated by VPM input to L4 and POm input to L5A

135 these nuclei, sharp-rising, large-amplitude EPSPs ("drivers") were not modulated by cortical slow wa

136 paraventricular hypothalamic neurons reduced EPSP duration, synaptic integration, and altered body we

137 EPSPS edits occurred at sufficient frequency that we cou

138 showed the expected Mendelian segregation of EPSPS edits.

139 powerful control over temporal summation of EPSPs, effectively suppressing low frequencies of parall

140 Almost every EPSP elicited a spike, but latency (300-1500 mus) varied

141 uration of principal cell discharges than DD EPSPs, enabling GCs to compare contrasting versions of o

142 ed by splanchnic nerve stimulation but not F-EPSPs evoked by colonic nerve stimulation.

143 ed by splanchnic nerve stimulation but not F-EPSPs evoked by colonic nerve stimulation.

144 ed by splanchnic nerve stimulation but not F-EPSPs evoked by colonic nerve stimulation.

145 stigmatellin potentiated the amplitude of F-EPSPs evoked by splanchnic nerve stimulation but not F-E

146 ne) significantly reduced the amplitude of F-EPSPs evoked by splanchnic nerve stimulation but not F-E

147 ifier, we have recorded unitary granule cell EPSPs evoked in response to mitral cell action potential

148 tively potentiated cholinergic fast EPSPs (F-EPSPs) evoked by splanchnic nerve stimulation but not F-

149 conductance and, during trains of simulated EPSPs, exhibited cumulative deactivation and inactivatio

150 H2S selectively potentiated cholinergic fast EPSPs (F-EPSPs) evoked by splanchnic nerve stimulation b

151 Unitary EPSPs failed to initiate a spike in CA3 neurons under co

152 We recorded the field EPSPs (fEPSPs) evoked at the CA3-CA1 synapse during the

153 sponse was observed consisting of a brief mf EPSP followed by an inhibitory response lasting on the o

154 Modelling suggested that summation of EPSPs from 18-24 tINs can make 20-50% of dINs fire.

155 old potentials like NMDA spikes or trains of EPSPs from dendrite to soma.

156 g as a gain control to suppress poorly timed EPSPs from generating postsynaptic APs to maintain preci

157 old potentials like NMDA spikes or trains of EPSPs from the distal apical dendrite to the soma in pyr

158 5-enolpyruvylshikimate 3-phosphate synthase (EPSPS) from the shikimate pathway, thereby causing delet

159 and other sources of large-amplitude unitary EPSPs, function to provide a timing signal linked to res

160 Fiber FISH displayed 10 copies of the EPSPS gene (approximately 5 kb) arranged in tandem confi

161 The EPSPS gene amplification was heritable in common waterhe

162 There was a positive correlation between EPSPS gene copies and its transcript expression.

163 se results suggest that the initial event of EPSPS gene duplication may have occurred because of uneq

164 (EPSPS) gene, with minor contributions from EPSPS gene duplication/overexpression.

165 ngle and prominent hybridization site of the EPSPS gene localized on the distal end of one pair of ho

166 ce in situ hybridization analysis mapped the EPSPS gene to pericentromeric regions of two homologous

167 -ENOYLPYRUVYLSHIKIMATE-3-PHOSPHATE SYNTHASE (EPSPS) gene and 58 other genes whose encoded functions t

168 5-enolpyruvylshikimate-3-phosphate synthase (EPSPS) gene in glyphosate-resistant individuals.

169 5-Enolpyruvylshikimate-3-Phosphate Synthase (EPSPS) gene, the enzyme target of glyphosate.

170 of the 5-enolpyruvylshikimate-3-P synthase (EPSPS) gene, which encodes the molecular target of glyph

171 5-enolpyruvylshikimate 3-phosphate synthase (EPSPS) gene, with minor contributions from EPSPS gene du

172 In glyphosate-resistant plants, a cluster of EPSPS genes on the pericentromeric region on one pair of

173 '-ENOLPYRUVYLSHIKIMATE-3-PHOSPHATE SYNTHASE (EPSPS) genes.

174 rug treatments that enhance the amplitude of EPSPs; however, drugs that alter the duration of the EPS

175 tic isotope effects (KIEs) on AroA-catalyzed EPSP hydrolysis, which also begins with a methylene carb

176 firing pattern modulated the size of unitary EPSPs impinging on NGFCs through FSI and not via a direc

177 Consistent with this idea, EPSPs in both cortical and hippocampal pyramidal neurons

178 the nociceptin-induced inhibition of evoked EPSPs in CeA neurons of naive rats.

179 mercial first generation glyphosate-tolerant EPSPS in corn (Zea mays) and now in other crops.

180 assive cable filtering during propagation of EPSPs in dendrites.

181 NPY strongly decreased stimulation-induced EPSPs in dentate gyrus and CA1 (up to 30 and 55%, respec

182 The timing of individual EPSPs in GC recordings also was phase modulated with the

183 Conotoxin GVIA abolished all EPSPs in inspiratory neurons from alpha(1A)(-)/(-) mice,

184 utons) from motoneurons, the reduction of IA EPSPs in motoneurons, and the disappearance of stretch r

185 Here, we show that APs and EPSPs in mouse hippocampal neurons trigger two spatially

186 designed to replicate in vivo recordings of EPSPs in muscle vasoconstrictor neurons, produced a 2.4-

187 ns caused suppression of subsequently evoked EPSPs in projection neurons.

188 n of corticothalamic neurons generated large EPSPs in pyramidal neurons in layer 5a.

189 ing presynaptic RSC axons evoked exclusively EPSPs in recorded postsynaptic layer V cells.

190 s to generate their characteristically large EPSPs in response to their cortical inputs; in contrast,

191 ecause EPSPs led APs in st-LTP while APs led EPSPs in st-LTD, STDP was Hebbian in nature.

192 er understand the interplay between bAPs and EPSPs in synaptic strength modification.

193 Only the fastest EPSPs in the ACC were reduced to a similar degree as in

194 imately 2-6 mV), monosynaptic, glutamatergic EPSPs in the hindbrain reticulospinal neurons (descendin

195 udes of excitatory post-synaptic potentials (EPSPs) in adult rat hippocampal slices.

196 d evoked excitatory postsynaptic potentials (EPSPs) in different cell-types across cortical layers in

197 endritic excitatory postsynaptic potentials (EPSPs) in hippocampal CA1 pyramidal neurons.

198 curtail excitatory postsynaptic potentials (EPSPs) in neuronal dendrites.

199 ylene carbon atom of phosphoenolpyruvate, or EPSP, in the reverse reaction.

200 Surprisingly, the mean voltage and peaks of EPSPs increased by only a few millivolts during trains.

201 are not mutually exclusive and SNX increases EPSPs independent of SK channel activity.

202 Analysis of mini-EPSPs indicated that these inhibitors had minimal postsy

203 ssociated with decreased NR2B expression and EPSP insensitivity to pharmacological blockade of NR2B,

204 annel function, had little effect on somatic EPSP integration, suggesting that this effect was due to

205 thus affect EPSP-spike coupling by altering EPSP integration.

206 post-synaptic excitatory synaptic potential (EPSP) integration in CA1 pyramidal cells.

207 erneuron firing pattern driven by individual EPSPs into a more regular spiking mode determined by the

208 ses during middle age and that this enhanced EPSP is maintained into late life, consistent with an ag

209 ring an action potential, represented by the EPSP, is a homeostatic set point that is precisely maint

210 Because EPSPs led APs in st-LTP while APs led EPSPs in st-LTD, S

211 d purinergic slow EPSPs and ATP-induced slow EPSP-like response in guinea pig submucosal plexus, sugg

212 Subthreshold EPSP-like waveforms also activated a large component of

213 When the dendrite is hyperpolarized, CF-EPSPs mainly activate T-type VGCCs, SK channels, and A-t

214 on event was detected when the modified rice EPSPS marker gene was inserted with the Ac transposon 5'

215 se direction in each of the 7 introns of the EPSPS marker gene.

216 nserted a Ds element into each intron of the EPSPS marker gene.

217 In GluRIIA mutant animals, miniature EPSP (mEPSP) amplitudes are significantly decreased, and

218 omputational simulations, we show that LANDD EPSPs more reliably encode the duration of principal cel

219 GSCs were sufficient to amplify subthreshold EPSPs near action potential threshold, counterbalancing

220 consecutive cycles of sound stimuli, somatic EPSP normalization renders spike initiation more sensiti

221 is dictated primarily by the kinetics of MF EPSPs, not feedforward inhibition.

222 recorded excitatory postsynaptic potentials (EPSPs) of regular (n =76) and all-or-none (n =24) type i

223 reasons why remaining IA synapses can evoke EPSPs on motoneurons, but fail to transmit useful stretc

224 otinic synapses produce large suprathreshold EPSPs on sympathetic and parasympathetic neurons to conv

225 rk demonstrated that hyperglycemia depresses EPSPs on sympathetic neurons and disrupts sympathetic re

226 -like EPSPs, others showing "modulator"-like EPSPs only.

227 owever, drugs that alter the duration of the EPSP or increase glutamate release lack efficacy.

228 ome revealing "driver"- and "modulator"-like EPSPs, others showing "modulator"-like EPSPs only.

229 gated STDP induction during low-frequency AP-EPSP pairing, with both LTP and LTD absent under control

230 reshold, counterbalancing the suppression of EPSP peaks by low voltage-activated potassium channels.

231 how individual quantal-sized corticothalamic EPSPs propagate within thalamocortical neuron dendrites

232 ng the afferent to potentials where a single EPSP (quantum) can generate an action potential.

233 Primary and secondary EPSPs recorded from the intact superior cervical ganglio

234 ) revealed reciprocal changes in spontaneous EPSP (sEPSP) frequency in male and female D1+ and D2+ MS

235 LANDD EPSPs show little depression in response to tetanic stim

236 The E. indica TIPS EPSPS showed very high-level (2,647-fold) in vitro resis

237 pike, but latency (300-1500 mus) varied with EPSP size and kinetics.

238 quantitatively for the marked difference in EPSP size.

239 iation of excitatory postsynaptic potential (EPSP)-spike coupling (E-S potentiation).

240 ly relevant, since long-term potentiation of EPSP-spike (E-S) coupling induced by the mGluR agonist w

241 Somatic K(V)7/M-channels thus affect EPSP-spike coupling by altering EPSP integration.

242 ngly, disruption of axonal channels enhanced EPSP-spike coupling by lowering the action potential thr

243 mice decreased dentate responses and shifted EPSP-spike coupling leftward after the shock zone was re

244 es to perforant-path stimulation and shifted EPSP-spike coupling leftward.

245 NMDAR antagonists decreased EPSPs and EPSP-spike coupling more strongly in pyramidal cells tha

246 The precise EPSP-spike coupling produced by fast-decaying EPSCs in F

247 omatic and axonal K(V)7/M-channels influence EPSP-spike coupling via different mechanisms.

248 Moreover, EPSP-spike coupling, a process that strongly influences

249 Here we show that EPSP-spike pairing at 6 Hz can optimally induce STDP at

250 coefficient of variation of the amplitude of EPSPs suggest a presynaptic action of serotonin.

251 perpolarization and conductance shunt during EPSP summation.

252 In cortical pyramidal neurons EPSP suppression by preceding APs depended on their prec

253 Five CP4 EPSPS surrogate peptides and their corresponding retenti

254 phate (EPSP) as a nonenzymatic analog of the EPSP synthase (AroA) reaction.

255 rotein (YFP) fused to the transit peptide of EPSP synthase* or the small subunit of Rubisco was not i

256 Because the EPSP synthase* pre-protein must be imported for its func

257 5-enolpyruvylshikimate 3-phosphate synthase (EPSP synthase*), a key enzyme in the shikimic acid pathw

258 r enolpyruvylshikimate 3-phosphate synthase (EPSP synthase, AroA) is protonating the methylene carbon

259 sate also contains an unreported Pro-106-Thr EPSPS target-site mutation.

260 B excite GCs by evoking potent nondepressing EPSPs (termed large-amplitude, nondendrodendritic [LANDD

261 tcomes: (1) feedforward inhibition or (2) an EPSP that elicited firing.

262 e at the soma of CA2 pyramidal neurons, with EPSPs that are 5-6 times larger than those in CA1 pyrami

263 imal dendrites usually produce large somatic EPSPs that efficiently trigger action potential (AP) out

264 threshold voltages produces amplification of EPSPs that is sensitive to the rate of depolarization an

265 n and, therefore, can be distinguished other EPSPs that target GCs.

266 ded with excitatory postsynaptic potentials (EPSPs) that maintained stable amplitudes when activated

267 1 dendritic properties limit the size of the EPSPs they generate, even to a similar number of cortica

268 Paired temporally with an EPSP, this Ca(2)(+) influx can result in synaptic plasti

269 upon cholinergic synaptic input and amplify EPSPs, thus indicating a conserved function of dendritic

270 uency of excitatory postsynaptic potentials (EPSPs) to TC cells, an increase in alpha power is needed

271 he rising slope of the EPSP and prolongs the EPSP-to-AP transition time.

272 unitary excitatory postsynaptic potentials (EPSPs) trigger spikes in CA3 neurons remains unknown.

273 reased the amplitude of both uncaging-evoked EPSPs (uEPSPs) and spine Ca transients.

274 whole-cell recordings to measure spontaneous EPSPs using a dual-channel template-matching algorithm t

275 ty of non-WFV cells, the amplitude of evoked EPSPs varied across trials.

276 al cells can elicit very large glutamatergic EPSPs (VLEs) in inhibitory GABAergic interneurons capabl

277 ent with the NR1 pattern, the NMDAR-mediated EPSP was smaller at 3 h and larger at 24 h.

278 The amplitude gradient of dendritic EPSPs was also apparent in responses to injections of id

279 Exonization of Ds in EPSPS was biased towards providing splice donor sites of

280 EPSPs was site-specifically immobilized on a transparent

281 The amplitude of evoked EPSPs was smaller in inspiratory neurons from alpha(1A)(

282 I(h), baseline sublinear summation of evoked EPSPs was unchanged in pyramidal neurons from HCN1 knock

283 5-enolpyruvylshikimate-3-phosphate synthase (EPSPS), was identified as the mechanism of glyphosate re

284 The amplitudes of EPSPs we characterized were smaller than those previousl

285 ngly, although mGlu7 agonists inhibit SC-CA1 EPSPs, we found no evidence for activation of mGlu7 by s

286 To address the mechanism, evoked EPSPs were analyzed revealing a greater proportion of sy

287 amics and temporal summation of burst-evoked EPSPs were cell-type dependent: in principal cells and s

288 athetic neurons and integration of nicotinic EPSPs were compared in primary cell culture and in the a

289 encies of synaptically evoked global APs and EPSPs were found to correspond to Deltat ~ 10 ms, explai

290 Optogenetically evoked HP EPSPs were greatly attenuated after a short latency (50

291 Splanchnic F-EPSPs but not colonic F-EPSPs were reduced in CSE knock-out (KO) mice.

292 al stretch, while still capable of eliciting EPSPs when synchronously fired by electrical volleys.

293 hase, from Agrobacterium sp. strain CP4 (CP4 EPSPS), which confers glyphosate tolerance in transgenic

294 Lagged cell EPSPs, which often derive from a single retinal input, h

295 corticothalamic inputs produce small somatic EPSPs whose amplitudes are passively normalized and virt

296 ression (LTD) normally caused by pairing 100 EPSPs with bursts of 2 bAPs evoked at a supracritical fr

297 Short-term plasticity of EPSPs with increasing frequency of presynaptic activity

298 EPSPs with segmental latency shorter than 1.2 ms were cl

299 phase preference imparted by large-amplitude EPSPs, with fast kinetics often matching the phase tunin

300 t to potentials at which smaller and smaller EPSPs would be sufficient to trigger APs.