ライフサイエンスコーパス: IPSC

1 IPSC latency and rise time were also strongly dependent

2 IPSC-derived human neurons, or iNs, hold promise for adv

3 IPSC-derived neural progenitor cells carrying the risk a

4 IPSCs and EPSCs show rapid acceleration during developme

5 IPSCs arriving in pairs of either pyramidal or fast-spik

6 IPSCs evoked from the NAc were potently inhibited by act

7 se in the brain through inhibition of GABA-A IPSCs onto dopamine cells.

8 Additional recordings of GABA-A IPSCs showed CRF-R2 activation-facilitated presynaptic r

9 revealed that the laserspritzer-induced AAS-IPSCs persisted in the presence of TTX and TEA but not 4

10 quency-dependent, slow STD (S-STD), adapting IPSC amplitudes in tens of seconds to minutes.

11 hibitory postsynaptic currents (IPSCs) along IPSC trains evoked by the 5 Hz electrical stimulation, b

12 tors, which prolonged the duration of alpha2-IPSCs when multiple release sites were activated synchro

13 relationship between subunit composition and IPSC decay is less clear.

14 al analysis of changes in miniature EPSC and IPSC properties in L2 pyramidal neurons showed that mEPS

15 During swimming, EPSC and IPSC rates increased.

16 Both EPSCs and IPSCs have slow kinetics in prehearing animals, which du

17 matures by postnatal day 20, with EPSCs and IPSCs having fast kinetics.

18 stimulation in either ear produced EPSCs and IPSCs in most neurons.

19 We recorded EPSCs and IPSCs to examine the buildup of neuronal activity preced

20 firing rates near 8 spikes/s, and EPSCs and IPSCs were evident.

21 EPSCs and IPSCs were well correlated except in center-preferred ne

22 ic currents (combined simultaneous EPSCs and IPSCs) became markedly depolarized during the preictal p

23 sity and in evoked and spontaneous EPSCs and IPSCs.

24 PSCs evoked from the RMTg, 18% from NAc, and IPSCs evoked from VTA interneurons were almost insensiti

25 either mCbN afferents or TH neurons augments IPSCs and suppresses EPSCs in Chx10 neurons by activatin

26 aptic current (IPSC) in a PN and an autaptic IPSC.

27 omputational analysis indicated that GABA(B) IPSCs can phasically modulate the discharge of PT intern

28 CB(1) receptor antagonists enhanced basal IPSCs in CA1 pyramidal neurons in MAGL(-)/(-) mice, whil

29 group II/III mGluR activation decreases both IPSC frequency and I(GABA)tonic amplitude.

30 concentration-dependent enhancement of both IPSC frequency and tonic GABA(A) current (I(GABA)tonic)

31 butes contrast with large cells, whose brief IPSCs and rapid firing rates can permit well timed posti

32 se, interneuronal excitability was high, but IPSCs, evoked by local stimulation, or osmotically by hy

33 In mutant CbN cells, IPSC kinetics were unchanged, but mutant males, unlike f

34 neurons, strong focal shocks evoked compound IPSCs indicating convergent summation of multiple inhibi

35 In contrast, IPSC amplitude did not differ between cell types.

36 ed than excitatory ones, but that correlated IPSCs arise from the activation of common presynaptic in

37 diated slow inhibitory postsynaptic current (IPSC) in a PN and an autaptic IPSC.

38 or-mediated inhibitory postsynaptic current (IPSC) that resulted in only a transient pause in firing.

39 uration and inhibitory postsynaptic current (IPSC).

40 al cells, we found that inhibitory currents (IPSCs) are more correlated than excitatory ones, but tha

41 ression of inhibitory postsynaptic currents (IPSCs) along IPSC trains evoked by the 5 Hz electrical s

42 ecrease in inhibitory postsynaptic currents (IPSCs) and an increase in the AMPAR/NMDAR ratio in ventr

43 e decay of inhibitory postsynaptic currents (IPSCs) and induce spontaneous GlyR activation.

44 ression of inhibitory postsynaptic currents (IPSCs) followed by modest long-term depression (I-LTD) i

45 2-receptor inhibitory postsynaptic currents (IPSCs) in GIRK2-expressing MSNs that occurred in under a

46 -frequency inhibitory postsynaptic currents (IPSCs) in pyramidal cells, even with glutamatergic trans

47 B-mediated inhibitory postsynaptic currents (IPSCs) in VTA dopamine neurons, and these effects were m

48 ression of inhibitory postsynaptic currents (IPSCs) induced by D(2) dopamine receptor and cannabinoid

49 of evoked inhibitory postsynaptic currents (IPSCs) mediated by D1-type receptors seen in wild-type m

50 miniature inhibitory postsynaptic currents (IPSCs) of lamina II neurons.

51 GABAergic inhibitory postsynaptic currents (IPSCs) recorded from neurons in the mouse ventral tegmen

52 otentiates inhibitory postsynaptic currents (IPSCs) specifically in perisomatic synapses.

53 ontaneous inhibitory post-synaptic currents (IPSCs) in MSNs.

54 nsmission (inhibitory postsynaptic currents, IPSCs) in the DR.

55 he guinea pig determined the duration the D2-IPSC.

56 Evoked D2-IPSCs could be driven by repetitive stimulation and were

57 Functionally, differences in D2-IPSCs resulted in inhibition of dopamine neuron firing o

58 dopamine D2-autoreceptor-mediated IPSCs (D2-IPSCs) in the VTA of mouse, rat, and guinea pig.

59 ime course of D2-receptor-mediated IPSCs (D2-IPSCs) was consistent between cells and was unaffected b

60 with cocaine extended the time course of D2-IPSCs and suggested that transporters strongly limited s

61 This resulted in an increased duration of D2-IPSCs in the guinea pig.

62 tributed independently to the duration of D2-IPSCs.

63 Robust D2-IPSCs were observed in all recordings from neurons in sl

64 urons in slices taken from mouse, whereas D2-IPSCs in rat and guinea pig were observed less frequentl

65 ors, was responsible for the slowly decaying IPSCs.

66 delta IPSCs decay slower than gamma2 IPSCs, but the reasons ar

67 delta IPSCs showed more sensitivity to altered transmitter rel

68 tude and decreased the decay of evoked delta IPSCs but had no effect on delta or dual-component (main

69 findings also reveal that spontaneous delta IPSCs are mainly driven by channel deactivation, rather

70 Overall, our results indicate that delta IPSCs are activated by both synaptic and diffusional GAB

71 estly more diffusional contribution to delta IPSCs.

72 prisingly, decreased depression of dendritic IPSCs isolated after blocking GABAa receptor on the soma

73 asynaptic delta subunits mediate diffusional IPSCs and tonic current.

74 vivo induction of AT at around P20 disrupted IPSC and EPSC integration in the LSO, so that 1 week lat

75 in perisomatic synapses, suggesting distinct IPSC decay kinetics.

76 Cholinergically driven IPSCs were not affected by ablation of striatal fast-spi

77 ency of spontaneous, action potential-driven IPSCs.

78 ine neurons from adult rats exhibit enhanced IPSCs after adolescent alcohol exposure corresponding to

79 aring Purkinje firing rates and eurydendroid IPSC rates indicated that 1-3 Purkinje cells converge on

80 complex spikes, suggested that eurydendroid IPSC size depended on presynaptic spike duration rather

81 ors by iontophoresis of ATP decreased evoked IPSC amplitudes and action potential-evoked calcium tran

82 Evoked IPSCs (eIPSCs) mediated by GABAA receptors were isolated

83 2 agonist but not D1 agonist, on both evoked IPSCs and EPSCs, were reduced.

84 uency spiking in single granule cells evoked IPSCs in approximately 5% of neighboring granule cells,

85 ative perisomatic, but not dendritic, evoked IPSCs were significantly reduced in these mice.

86 developmental period also facilitated evoked IPSCs in CA1 neurons, while evoked IPSCs and miniature I

87 ta3-KO mice exhibited attenuated GABA-evoked IPSCs.

88 In this preparation, light-evoked IPSCs could only reach axotomized BC terminals via the l

89 d a unique preparation to study light-evoked IPSCs recorded from axotomized terminals of ON-type mixe

90 ta, agonists reduced the amplitude of evoked IPSCs and appeared to colocalize in a significant portio

91 proximately 70%; (2) the amplitude of evoked IPSCs and isoguvacine-evoked current increased by approx

92 Cs, whereas the paired-pulse ratio of evoked IPSCs was unaffected, suggesting that the absence of Cx3

93 ell axon collaterals had no effect on evoked IPSCs measured in synaptically coupled Purkinje cells.

94 ion of AgRP neurons reliably produced evoked IPSCs in POMC neurons, leading to the inhibition of POMC

95 ytosis is not apparent when recording evoked IPSCs in the presence of AM251, suggesting that the exoc

96 ctivation of receptors contributed to evoked IPSCs, serotonin reuptake transporters prevented pooling

97 ed evoked IPSCs in CA1 neurons, while evoked IPSCs and miniature IPSC amplitude were reduced followin

98 rs in mouse dentate granule cells to explore IPSCs.

99 ne in GlyT2-Cre transgenic mice, evoked fast IPSCs in principal cells.

100 ming on the scale of milliseconds, only fast IPSCs can enhance the detection of narrowband acoustic s

101 ON and OFF L-IPSCs, like reciprocal feedback IPSCs, were mediated by both GABA(A) and GABA(C) recepto

102 Consistent with these findings, IPSCs recorded from high-frequency OHCs that express BK

103 ing a switch from Glyalpha2 to Glyalpha1 for IPSCs and increased expression of GluA3 and GluA4 subuni

104 The low-frequency IPSC oscillations induced by CCh or optogenetically stim

105 wever, this had no effect on theta-frequency IPSC rhythms induced by carbachol (CCh).

106 had no effect on evoked or spontaneous GABA IPSCs.

107 D1)-mediated long-term potentiation of GABAA-IPSCs (D1-LTPGABA) in the oval bed nucleus of the stria

108 ted inhibitory postsynaptic currents (GABAAR IPSCs) is associated with reduced EtOH consumption.

109 st robust DPDPE-induced inhibition of GABAAR IPSCs in VTA neurons.

110 ulation of drinking and inhibition of GABAAR IPSCs, we examined whether these changes can be predicte

111 (p = 0.003, n = 26) and augmented GABAergic IPSCs in CVNs by 21 +/- 5% (p = 0.001, n = 26).

112 on of VP neuron terminals elicited GABAergic IPSCs in both dopamine (DA) and non-DA VTA neurons, and

113 TRN neurons and their axons evokes GABAergic IPSCs in TRN neurons in mice younger than 2 weeks of age

114 UBC relay, whereas large and fast GABAergic IPSCs may in addition control spike timing in mGluRII-ne

115 rginine nor SNAP had any effect on GABAergic IPSCs.

116 ubtypes of type 2 PG cells receive GABAergic IPSCs from the basal forebrain but not from other PG cel

117 st-spiking interneurons, recurrent GABAergic IPSCs predominated interictally and during the early pre

118 eased the frequency of spontaneous GABAergic IPSCs without changes in their amplitudes.

119 Surprisingly, unitary GABAergic IPSCs were only weakly calcium dependent.

120 increase in glycinergic, but not GABAergic, IPSCs in CVNs.

121 ion, we find that in general delta and gamma IPSCs are modulated in parallel by manipulations of tran

122 delta IPSCs decay slower than gamma2 IPSCs, but the reasons are unclear.

123 isetron, significantly increases glycinergic IPSC decay times without causing motor side effects.

124 eptor (NMDAR)-mediated EPSCs and glycinergic IPSCs.

125 Interestingly, SOD GABAergic/glycinergic IPSCs and evoked GABA(A)R-currents exhibited a slower de

126 reased the frequency of isolated glycinergic IPSCs by 27 +/- 8% (p = 0.003, n = 26) and augmented GAB

127 shed the effect of L-arginine on glycinergic IPSCs but not on evoked monosynaptic EPSCs.

128 We propose that slow glycinergic IPSCs may provide an inhibitory tone, setting the gain o

129 We show that glycinergic IPSCs are present in all cells.

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

131 pting pyramidal neurons, and also had higher IPSC and EPSC frequencies than adapting neurons.

132 However, IPSC decays evoked by axo-axonic, parvalbumin- or cholec

133 local release of serotonin generated 5-HT1A -IPSCs in serotonin neurons that rose and fell within a s

134 As a result, the decay of 5-HT1A -IPSCs was independent of the intensity of stimulation or

135 The duration of 5-HT1A -IPSCs was primarily shaped by receptor deactivation due

136 ed inhibitory postsynaptic currents (5-HT1A -IPSCs) generated by the activation of G-protein-coupled

137 extrasynaptic space from activating 5-HT1A -IPSCs.

138 holinergic-evoked inhibition, and a delay in IPSC latency.

139 This led to substantial increases in IPSC activity among WT relay neurons but had little impa

140 We also rule out small increases in IPSC decay times (as caused by W170S and R414H) as a pos

141 by the inefficiency of carbachol to increase IPSC frequency in these cells.

142 notropic GluRs and nAChRs blocked, increased IPSCs in MTCs and ETCs, indicating that mAChRs recruit g

143 of adenosine receptors selectively increased IPSCs evoked from the NAc during morphine withdrawal.

144 Rs in the presence of tetrodotoxin increased IPSCs in all glomerular neurons, indicating action poten

145 The Abeta-induced IPSC decline could be prevented with intracellular appli

146 activation accounted for 15% of interneuron IPSC amplitude, while the remaining current was mediated

147 This biphasic form of L-IPSC plasticity may underlie adaptation and sensitizatio

148 rvals (PPIs) of 50 and 300 ms, whereas OFF L-IPSC latencies decreased at the 300 ms PPI.

149 erm plasticity of GABAergic lateral IPSCs (L-IPSCs).

150 stic changes in the strength and timing of L-IPSCs help to dynamically shape the time course of gluta

151 Short-term plasticity of L-IPSCs may thus influence the strength, timing, and spati

152 Bright light stimulation evoked ON and OFF L-IPSCs in axotomized BCs, which had distinct onset latenc

153 depression at intervals <1 s, whereas OFF L-IPSCs showed depression at intervals </=1 s and amplitud

154 AMPARs differentially affected ON and OFF L-IPSCs, confirming that these two types of feedback inhib

155 ON and OFF L-IPSCs, like reciprocal feedback IPSCs, were mediated by

156 paired light stimulation, latencies of ON L-IPSCs increased at paired-pulse intervals (PPIs) of 50 a

157 ON L-IPSCs showed paired-pulse depression at intervals <1 s,

158 h the synaptic strength and latency of the L-IPSCs.

159 e short-term plasticity of GABAergic lateral IPSCs (L-IPSCs).

160 ing alpha-subunit of BK channels have longer IPSCs than do the OHCs of BKalpha(+/+) littermates.

161 mputational modelling confirmed that matched IPSC and EPSC kinetics are required to generate mature i

162 irmed that basal forebrain afferents mediate IPSCs on granule and deep short axon cells.

163 ong-lasting enhancement of feedback-mediated IPSC/Ps in the projection neurons, which persists for th

164 resulting dopamine D2-autoreceptor-mediated IPSCs (D2-IPSCs) in the VTA of mouse, rat, and guinea pi

165 mate-mediated EPSCs as well as GABA-mediated IPSCs, although the net effect of neurotransmitter relea

166 harmacological correction of gamma2-mediated IPSCs with diazepam restored total EEG power toward base

167 dependent currents, slower Purkinje-mediated IPSCs, and lower spontaneous firing rates, but rotarod p

168 rea, the time course of D2-receptor-mediated IPSCs (D2-IPSCs) was consistent between cells and was un

169 ged the duration of alpha2-receptor-mediated IPSCs even when reuptake was intact.

170 GABA(A) receptor-mediated IPSCs evoked by electrical or optogenetic stimulation of

171 , and monosynaptic GABA(A) receptor-mediated IPSCs were elicited.

172 A1 neurons, while evoked IPSCs and miniature IPSC amplitude were reduced following astrocytic ephrin-

173 led a reduction in spontaneous and miniature IPSC frequency after head injury; no concurrent change i

174 hibitory short-term plasticity and miniature IPSC frequency and amplitude were normal in Cntnap2(-/-)

175 rong positive relationship between miniature IPSC frequency and the occurrence of both stereotyped ex

176 Miniature IPSCs in Cre(+) PCs were insensitive to low concentratio

177 evious reports of larger amplitude miniature IPSCs and larger BC-->GC quantal size.

178 n the frequency of spontaneous and miniature IPSCs, an effect completely abolished by the GABAA recep

179 Moreover, FS-->SP evoked miniature IPSCs increased in deprived hemispheres when MD was init

180 adjuvant (CFA) increased GABAergic miniature IPSCs (mIPSCs).

181 nsities of spontaneous glycinergic miniature IPSCs (mIPSCs) were significantly smaller in the G93A-SO

182 miniature EPSCs with no change in miniature IPSCs, indicating that overexpression of MeCP2 selective

183 miniature EPSCs and interestingly, miniature IPSCs.

184 changes in inhibition by measuring miniature IPSCs (mIPSCs) in layer 2/3 pyramidal neurons of mouse v

185 verage amplitude of GABAA-mediated miniature IPSCs (mIPSCs) in these neurons is enhanced for several

186 less frequent spontaneous but not miniature IPSCs.

187 combining whole-cell recordings of miniature IPSCs (mIPSCs) and quantitative immunolocalization of sy

188 er Cd(2+) reduced the frequency of miniature IPSCs (mIPSCs) in granule cells by approximately 50%, su

189 Specifically, the amplitude of miniature IPSCs (mIPSCs) was decreased after 21 d withdrawal from

190 icantly increased the frequency of miniature IPSCs (mIPSCs).

191 andamide increase the frequency of miniature IPSCs (mIPSCs)recorded from hilar mossy cells without al

192 ecordings revealed the presence of miniature IPSCs in Cre(+) layer 2/3 pyramidal cells (PCs) with unc

193 ted the amplitude distributions of miniature IPSCs, whereas the paired-pulse ratio of evoked IPSCs wa

194 ects of ex vivo ethanol (50 mM) on miniature IPSCs (mIPSCs) in the DR 24-h post-ethanol exposure.

195 ing amplitude and had no effect on miniature IPSCs or EPSCs.

196 equency of tetrodotoxin-resistant, miniature IPSCs (mIPSCs) in 67% of DMV neurons recorded in acutely

197 in-, and 4-aminopyridine-sensitive miniature IPSCs (mIPSCs) mediated by GABA(A) receptors.

198 ons without changes in spontaneous miniature IPSCs (mIPSCs).

199 but less well than the summation of monaural IPSCs.

200 minimal focal shocks activated monosynaptic IPSCs at fixed latency (low jitter) that often failed (3

201 , LSP4-2022 also reduced evoked monosynaptic IPSCs in CA1 pyramidal cells and, in contrast to its eff

202 ergic LH --> PVH fibers induced monosynaptic IPSCs in PVH neurons, and potently increased feeding, wh

203 sted DMV preganglionic neurons (PGNs) but no IPSCs.

204 -Astrocyte autaptic evoked EPSCs, but not IPSCs, displayed an altered temporal profile, which incl

205 . WT neurons and a DPDPE-induced decrease of IPSC frequency revealed a role for DOPs.

206 In the dLGN, enhancement of IPSC frequency and I(GABA)tonic by group I mGluRs is not

207 Inhibition of IPSC frequency by morphine was also reduced in beta-arr2

208 5 subtypes, the mGluR-dependent component of IPSCs elicited by intrastriatal electrical stimulation i

209 gamma2 and delta components of IPSCs were modulated similarly by presynaptic manipulati

210 s demonstrate that diversity in the decay of IPSCs can be generated by varying the expression of diff

211 Cs and a 5.3-fold difference in the decay of IPSCs elicited by single-pulse stimulus.

212 llular Ca2+ with Sr2+ increased the decay of IPSCs in LF neurons, and EGTA-AM reduced the decay of IP

213 LF neurons, and EGTA-AM reduced the decay of IPSCs in MF/HF neurons.

214 rons (PV-IPSCs), but decreased depression of IPSCs from dendritically projecting somatostatin cells (

215 ic analyses revealed increased depression of IPSCs originating from perisomatically projecting parval

216 CB(1) receptor agonist-induced depression of IPSCs was decreased in MAGL(-)/(-) mice.

217 arly component of DHPG-induced depression of IPSCs was mediated by the cannabinoid CB1 receptors, whi

218 The facilitation of IPSCs produced by direct cAMP stimulation was unaffected

219 lient observation was a reduced frequency of IPSCs and EPSCs, whereas the amplitudes were not modifie

220 These data suggest that inhibition of IPSCs by morphine involves a beta-arr2/c-Src mediated me

221 Morphine induced a 46% inhibition of IPSCs evoked from the RMTg, 18% from NAc, and IPSCs evok

222 d, moreover, show that the decay kinetics of IPSCs are slowed in mature animals.

223 The kinetics of IPSCs influence many neuronal processes, such as the fre

224 p recordings, the amplitudes and kinetics of IPSCs mediated by AASs were similar to those mediated by

225 By examining the decay kinetics of IPSCs, we found that while spillover may allow for the a

226 Furthermore, the reversal potential of IPSCs, which was not significantly altered during withdr

227 Our data demonstrate the presence of IPSCs and the synaptic enrichment of the alpha1 and beta

228 ptors matches the pharmacological profile of IPSCs.

229 The simultaneous reduction of IPSCs and increase in membrane resting potential produce

230 ion that, through the timing and strength of IPSCs and EPSCs, produces sparse and reliably timed cort

231 jected into an ET cell evoked suppression of IPSCs.

232 ased, suggesting that the relative timing of IPSCs and EPSCs may permit excitation to drive additiona

233 ation frequency was only weakly dependent on IPSC amplitude, and decreased to that of CA3 slow gamma

234 enhanced the DOP receptor-induced effect on IPSCs via presynaptic mechanisms.

235 However, there was little or no effect on IPSCs.

236 AZD7325 demonstrates stronger effects on IPSCs in the seizure resistant mouse strain, consistent

237 principal cells paced by recurrent perisomal IPSCs.

238 nergic nerve endings to mediate fast, phasic IPSCs.

239 -containing GABA(A) receptors mediate phasic IPSCs while extrasynaptic delta subunits mediate diffusi

240 -R2 agonists to depress EPSCs and potentiate IPSCs was diminished.

241 Zolpidem prolongs IPSCs to decrease sleep latency and increase sleep time,

242 ally projecting parvalbumin interneurons (PV-IPSCs), but decreased depression of IPSCs from dendritic

243 sed the sensitivity of SOM-IPSCs, but not PV-IPSCs to a GABAb receptor agonist baclofen.

244 iation to an increase in the size of quantal IPSC, suggesting a strengthening of the postsynaptic res

245 quency stimulation of SC afferents to reduce IPSC amplitudes.

246 reased to that of CA3 slow gamma by reducing IPSC decay rate or reducing interneuron activation throu

247 also known as Kir3) channels mediate a slow IPSC and control the excitability of DA neurons.

248 Although fast and slow IPSCs in T-stellate cells improve spike timing on the sc

249 mulation evokes large GABA(B)R-mediated slow IPSCs in perisomatic-targeting (PT) PVIs, but only small

250 pus, where they prolong the duration of slow IPSCs in pyramidal cells.

251 tero-oligomers increase the duration of slow IPSCs.

252 Computer models reveal that slow IPSCs in bushy cells can improve spike timing on the sca

253 -CF (MF/HF) neurons had significantly slower IPSCs, with a 2.6-fold difference in the decay time cons

254 surface expression was reflected by smaller IPSCs, which may underlie the induction of seizures.

255 ritically projecting somatostatin cells (SOM-IPSCs).

256 anwhile, OF decreased the sensitivity of SOM-IPSCs, but not PV-IPSCs to a GABAb receptor agonist bacl

257 Our results suggest that target-specific IPSC kinetics are critical for the segregated parallel p

258 tion to prolonging miniature and spontaneous IPSC interevent intervals, brain injury significantly re

259 i), our results showed increased spontaneous IPSC frequency and amplitude in MSNs as well as in the m

260 TRH increased spontaneous IPSC frequency without affecting amplitude and had no ef

261 Morphine inhibited spontaneous IPSC frequency, mainly through MOPs, with only a negligi

262 vealed rhythmic, large amplitude spontaneous IPSCs that had a similar frequency, pattern and opioid s

263 and alters cell capacitance and spontaneous IPSCs amplitude of AVPV/PeN and Arc Kiss1 populations in

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

265 ceptors similar to that of delta spontaneous IPSCs, consistent with the idea that deactivation and lo

266 d local GABA actions drive delta spontaneous IPSCs.

267 component (mainly gamma2-driven) spontaneous IPSCs, suggesting that GABA actions can be local for bot

268 principal neurons, and increased spontaneous IPSCs recorded from principal cells significantly more t

269 GABA-mediated spontaneous IPSCs (sIPSCs) in POMC neurons were unaffected by distur

270 Indeed, the frequency of spontaneous IPSCs (sIPSCs) onto POMC neurons increases during calori

271 nd reduction in the amplitude of spontaneous IPSCs (sIPSCs).

272 e in the decay time constants of spontaneous IPSCs and a 5.3-fold difference in the decay of IPSCs el

273 rpine increased the frequency of spontaneous IPSCs in CA1 pyramidal neurons >twofold (KA: P = 0.04; p

274 pirole, whereas the amplitude of spontaneous IPSCs was increased by quinpirole but not dopamine.

275 uced at P12-13, whereas those of spontaneous IPSCs were significantly increased at P12-13; and (5) bo

276 ptors inhibited the frequency of spontaneous IPSCs.

277 a-ARs increased the frequency of spontaneous IPSCs; however, this effect was smaller and confined to

278 ABA transporter has no effect on spontaneous IPSCs recorded in TRN neurons aged 2 weeks or older whil

279 lation at 20-150 Hz evoked greatly summating IPSCs.

280 depolarizing steps significantly suppressed IPSCs induced by application of the cholinergic agonist

281 Cs that express BK channels are briefer than IPSCs recorded from low-frequency (apical) OHCs that do

282 Our results show that IPSCs are less frequent in SOD animals in accordance wit

283 The IPSC difference between pyramidal subtypes was activity

284 In contrast, the IPSC decay time constant depended only on the postsynapt

285 was elevated by an amount expected from the IPSC alteration.

286 The IPSCs are regulated by exogenous and endogenous cannabin

287 onged the rise and reduced the amplitude the IPSCs and the effects were potentiated when uptake was i

288 Bath-applied Abeta (1 mum) depressed the IPSCs on average to 60% of control, whereas a reversed s

289 tro, it evoked a transient depression of the IPSCs.

290 lover plays a greater role in prolonging the IPSCs of MF/HF neurons.

291 These IPSCs then decreased to zero or reversed polarity by the

292 amine (DA) and non-DA VTA neurons, and these IPSCs were inhibited by the mu opioid receptor agonist D

293 The slow kinetics of these IPSCs was likely caused by the low concentration and spi

294 we show that the waveform of randomly timed IPSCs (evoked by high extracellular potassium) in high-f

295 ation profile of agonists underlying the two IPSCs.

296 o measured kinetic properties of the unitary IPSC: latency, rise time, and decay time constant.

297 Furthermore, unitary IPSCs recorded at IS3-OLM synapses had a small amplitude

298 1 at GABAergic synapses, we recorded unitary IPSCs (uIPSCs) at cholecystokinin-expressing interneuron

299 ch differences were especially dramatic when IPSCs were elicited by train stimulations at physiologic

300 of presynaptic adenosine receptors, whereas IPSCs evoked from RMTg were not changed.