ライフサイエンスコーパス: EPSP

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

2 s during excitatory postsynaptic potentials (EPSPs).

3 red with excitatory postsynaptic potentials (EPSPs).

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

5 ntibody occluded the SNX-induced increase of EPSPs.

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

7 related to nested bursts of theta-frequency EPSPs.

8 tion neurons were not able to inhibit evoked EPSPs.

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

10 ic corticospinal neurons had faster decaying EPSPs.

11 s result in the largest and sharpest somatic EPSPs.

12 n potentials evoked by single AMPA-dependent EPSPs.

13 coincidence of the rising slopes of unitary EPSPs.

14 et firing was triggered by IPSPs rather than EPSPs.

15 l or cortical stimulation with glutamatergic EPSPs.

16 e initiation and by subthreshold boosting of EPSPs.

17 ally efficient, glyphosate-resistant class I EPSPS.

18 voltage of stronger, but still subthreshold, EPSPs.

19 een postsynaptic action potentials (APs) and EPSPs.

20 hrough comparisons of the relative timing of EPSPs.

21 amplification of integrated corticothalamic EPSPs.

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

23 rneurons, BFc inputs elicited fast nicotinic EPSPs.

24 mutation to create the highly resistant TIPS EPSPS.

25 gain by inhibiting summation of subthreshold EPSPs.

26 potentials or on the frequency of miniature EPSPs.

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

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

29 endritic excitatory postsynaptic potentials (EPSPs) accelerated membrane repolarization in a voltage-

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

31 cted the region of space evoking the largest EPSP, across the population, synaptic inputs enforced a

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

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

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

35 itochondrial membrane potential and of field EPSPs after transient OGD, and combined removal of Ca(2+

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

37 drop in spike threshold triggered by larger EPSPs, allowing them to fire time-locked spikes in respo

38 EPSPs also could be amplified by the Na conductance when

39 f VGSCs from the dendrites equalizes somatic EPSP amplification across synaptic locations and lowered

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

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

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

43 EPSP amplification was restricted to the perisomatic reg

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

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

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

47 EPSP amplitude changes were correlated with changes of r

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

49 Changes in EPSP amplitude distributions in dual recordings were con

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

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

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

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

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

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

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

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

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

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

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

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

62 old EPSPs that behaved paradoxically in that EPSP amplitudes increased with intensity, even though bi

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

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

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

66 esponded to different stimuli with increased EPSP amplitudes.

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

68 excessive depolarization by the monosynaptic EPSP and multiple action potential firings.

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

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

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

72 otentiation arose from shunting of dendritic EPSPs and APs.

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

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

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

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

77 ly evoked Ca(2+) influx to limit the size of EPSPs and spine Ca(2+) transients.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

100 The shape indices of these EPSPs are tuned to transmit the information from each ax

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

102 Na conductance in AII amacrines accelerated EPSPs arising from RB synaptic input.

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

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

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

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

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

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

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

110 EPSP bursts were able to trigger afferent spikes, which

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

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

113 olarizing effect on the peak voltage of weak EPSPs, but produced a paradoxical hyperpolarizing effect

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

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

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

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

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

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

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

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

122 pies besides the native chromosome pair with EPSPS copies.

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

124 subthreshold activity was panoramic in that EPSPs could be evoked from all locations in all cells.

125 ed and suggest that the ipsilaterally evoked EPSPs could influence the responsiveness of IC cells to

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

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

128 er the stimulus, even on trials in which the EPSP did not directly trigger a spike.

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

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

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

132 EPSPS edits occurred at sufficient frequency that we cou

133 showed the expected Mendelian segregation of EPSPS edits.

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

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

136 EPSPS enzyme activity from resistant and susceptible pla

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

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

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

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

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

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

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

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

145 Quantitative RT-PCR on cDNA revealed that EPSPS expression was positively correlated with genomic

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

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

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

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

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

151 on, the molecular basis for GA21 corn, using EPSPS from E. coli.

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

153 5-enolpyruvylshikimate 3-phosphate synthase (EPSPS) from the shikimate pathway, thereby causing delet

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

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

156 The EPSPS gene amplification was heritable in common waterhe

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

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

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

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

161 PCR to measure relative copy numbers of the EPSPS gene.

162 5-enolpyruvylshikimate-3-phosphate synthase (EPSPS) gene in glyphosate-resistant individuals.

163 5-Enolpyruvylshikimate-3-Phosphate Synthase (EPSPS) gene, the enzyme target of glyphosate.

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

165 nnels also limited the temporal summation of EPSPs, generated through two-photon uncaging of glutamat

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

167 FISH revealed that EPSPS genes were present on every chromosome and, theref

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

169 sed EPSPS protein level also correlated with EPSPS genomic copy number.

170 Na channel-mediated effects on EPSPs, however, appeared to occur at the single-cell rat

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

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

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

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

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

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

177 assive cable filtering during propagation of EPSPs in dendrites.

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

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

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

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

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

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

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

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

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

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

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

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

190 es of coordinating axons caused large, brief EPSPs in their targets.

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

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

193 hreshold excitatory postsynaptic potentials (EPSPs) in mouse CA1 hippocampal neurons.

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

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

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

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

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

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

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

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

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

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

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

205 5-enolpyruvylshikimate-3-phosphate synthase (EPSPS) is the target of the broad spectrum herbicide gly

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

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

208 The genetic engineering of EPSPS led to the introduction of glyphosate-resistant cr

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

225 synaptic depolarization that can result from EPSPs paired with action potentials or larger EPSPs that

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

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

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

229 Immunoblot analyses showed that increased EPSPS protein level also correlated with EPSPS genomic c

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

231 The mean peak amplitude of EPSPs recorded from pairs of L2/3 neurons ranged between

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

233 he threshold dynamics associated with larger EPSPs reduced the probability of firing spikes outside o

234 ssion was positively correlated with genomic EPSPS relative copy number.

235 EPSP rise times were consistent with the majority of the

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 e largest EPSP, we observed a slowing in the EPSP slope along the contralateral-ipsilateral plane tha

240 SR field EPSP slopes were unaffected by SLM prepulses.

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

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

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

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

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

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

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

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

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

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

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

252 d, was created by point mutations of class I EPSPS, such as the enzymes from Zea mays or Escherichia

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

254 perpolarization and conductance shunt during EPSP summation.

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

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

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

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

259 5-enolpyruvylshikimate 3-phosphate synthase (EPSP synthase*), a key enzyme in the shikimic acid pathw

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

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 lls, ipsilateral signals evoked subthreshold EPSPs that behaved paradoxically in that EPSP amplitudes

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

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

266 PSPs paired with action potentials or larger EPSPs that trigger dendritic spikes.

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 was reflected in a temporal sequence of peak EPSP times.

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

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

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

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

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

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

281 to NMDA receptor-mediated components of the EPSPs was substantially increased after inducing potenti

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 f the sound location that evoked the largest EPSP, we observed a slowing in the EPSP slope along the

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

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

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

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

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

294 5-enolpyruvylshikimate-3-phosphate synthase (EPSPS), while the other four herbicides contain differen

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.