ライフサイエンスコーパス: long-term potentiation

1 sufficient to mimic the effects of stress on long-term potentiation.

2 spine formation, neuronal facilitation, and long-term potentiation.

3 electrophysiologic deficits such as reduced long-term potentiation.

4 the hippocampus and neocortex, compromising long-term potentiation.

5 reduction of persistent spines, and impaired long-term potentiation.

6 ted inhibition and excitation in hippocampal long-term potentiation.

7 Abeta) oligomers on synapses and hippocampal long-term potentiation.

8 BDNF receptor tyrosine kinase TrkB to elicit long-term potentiation.

9 ned the impact of postnatal loss of Mef2c on long-term potentiation.

10 ndrites and impaired theta burst stimulation long-term potentiation.

11 fter TBI and rescues deficits in hippocampal long-term potentiation.

12 uced glutamatergic synaptic transmission and long-term potentiation.

13 f PAG afferents in vitro unexpectedly causes long-term potentiation.

14 decrease of NMDAR clusters and impairment of long-term potentiation.

15 not alter baseline synaptic transmission or long-term potentiation.

16 es functional deficits of spatial memory and long-term potentiation.

17 naptic changes that characterize well-known, long-term potentiation, a strengthening of existing syna

18 mission, which is excitatory, and suppresses long-term potentiation, a surrogate of learning and memo

19 of Crmp2 in the hippocampus leads to reduced long-term potentiation, abnormal NMDA receptor compositi

20 y noradrenaline offers a novel mechanism for long-term potentiation ABSTRACT: Noradrenaline (NA) is a

21 enriched environment but also caused loss of long-term potentiation after theta-burst stimulation.

22 acid type A receptors attenuated deficits in long-term potentiation after traumatic brain injury.

23 d neurotrophic factor and impair hippocampal long-term potentiation, an electrophysiologic correlate

24 rious hippocampal subfields exhibit impaired long-term potentiation, an electrophysiological correlat

25 ion of PDE4A5 in hippocampal neurons impairs long-term potentiation and attenuates the formation of h

26 Spike timing-dependent long-term potentiation and depression (st-LTP and st-LTD

27 Long-term potentiation and depression of synaptic activi

28 ways responsible for synaptic vesicle cycle, long-term potentiation and depression, and neurotrophin

29 ed response inhibition through age-dependent long-term potentiation and depression-like plasticity me

30 ic plasticity genes that are both induced by long-term potentiation and downregulated in the aged bra

31 correlate with IQ and are thought to promote long-term potentiation and enhance memory consolidation.

32 ent with synaptic changes including enhanced long-term potentiation and impaired depotentiation ex vi

33 te-type glutamate receptor (NMDAR)-dependent long-term potentiation and long-term depression in USP6

34 spine structural plasticity during chemical long-term potentiation and long-term depression.

35 campal slices revealed significantly reduced long-term potentiation and long-term depression.

36 brain prevents the stabilization of synaptic long-term potentiation and markedly impairs long-term fe

37 cAMP is known to contribute to long-term potentiation and memory formation by controlli

38 s, pre- and postsynaptic structural defects, long-term potentiation and miniature postsynaptic curren

39 ed genes were enriched in calcium signaling, long-term potentiation and neuroactive ligand-receptor i

40 Knockdown of brain FNDC5/irisin impairs long-term potentiation and novel object recognition memo

41 ates that IH exposure attenuates hippocampal long-term potentiation and reduces adult neurogenesis.

42 nd connectivity with progressive deficits in long-term potentiation and spatial memory function.

43 nase C isoform, is important for maintaining long-term potentiation and storing memory.

44 nd decreased expression of genes involved in long-term potentiation and synaptic transmission, cancer

45 Glutamine increased the NMDAR-dependent long-term potentiation and the isolated NMDAR potentials

46 ificantly enhanced Abeta's ability to impair long-term potentiation and, upon intrahippocampal inject

47 ng plasticity in the indirect pathway toward long-term potentiation (and possibly also through more c

48 of T-type currents prevents the induction of long-term potentiation, and also interferes with long-la

49 ctivation, synaptic deficits, suppression of long-term potentiation, and cognitive impairment as comp

50 egration, spike timing-dependent plasticity, long-term potentiation, and learning.

51 c and axo-spinous synapses, was incapable of long-term potentiation, and less effectively patterned S

52 uch as phototriggered short-term plasticity, long-term potentiation, and neural facilitation.

53 actor of activated T cells (NFAT) signaling, long-term potentiation, and responsiveness to adrenergic

54 of brain slices with TIMP2 antibody prevents long-term potentiation, arguing for previously unknown r

55 KO mice, and they also exhibited attenuated long-term potentiation as well as deficits in spatial na

56 his betaAR signaling via Epac is involved in long term potentiation at cerebellar granule cell-to-Pur

57 unctionally, only patients' NMDAR-Ab prevent long-term potentiation at glutamatergic synapses, while

58 ynaptic transmission and decreased levels of long-term potentiation at hippocampal Schaffer collatera

59 discover a presynaptically expressed form of long-term potentiation at mossy cell outputs, shedding l

60 We show that optogenetic induction of long-term potentiation at perforant path synapses of den

61 erm depression and blunted depotentiation of long-term potentiation at the Schaffer collateral/cornu

62 rtance of OXTR signaling in the induction of long-term potentiation at the synapses between the entor

63 mice displayed a defect in the induction of long-term potentiation, but not long-term depression, at

64 aptic-related proteins, and disrupt chemical long-term potentiation (cLTP).

65 and concomitantly rescues their hippocampal long-term potentiation deficit.

66 chanism controlling synaptic strength during long-term potentiation/depression and homeostatic scalin

67 erm plasticity with heterogeneity, including long-term potentiation/depression and spike-timing-depen

68 biological synapses: unilateral connection, long-term potentiation/depression, a spike-timing-depend

69 nd large eCB transients produce eCB-mediated long-term potentiation (eCB-tLTP).

70 (FET) exhibits photo-induced short-term and long-term potentiation, electrically driven long-term de

71 ate that Dkk1 triggers synapse loss, impairs long-term potentiation, enhances long-term depression, a

72 mes: fluorescence analysis of single-synapse long-term potentiation (FASS-LTP).

73 aloric state of male rats, seesawing between long-term potentiation (iLTP, fed) and depression (iLTD,

74 and restore diminished levels of hippocampal long term potentiation in AD mice.

75 ts axonal growth, synaptic connectivity, and long-term potentiation in an APP-dependent manner.

76 ings of excitatory postsynaptic currents and long-term potentiation in brain slices and assessing the

77 ever, chronic NB-360 treatment did not alter long-term potentiation in CA1 neurons of Sez6(-/-) mice.

78 ophysiological experiments revealed enhanced long-term potentiation in hippocampal CA1 in the juvenil

79 synaptic plasticity, manifested by impaired long-term potentiation in hippocampal neurons, was also

80 U0409551 enhances NMDAR function and rescues long-term potentiation in hippocampal slices obtained fr

81 ndicates that these connections may underpin long-term potentiation in M1, our findings may lead to n

82 near-complete loss of spike-timing-dependent long-term potentiation in medium spiny neurons (MSNs).

83 Mice exposed to cNIC exhibited long-term potentiation in response to high-frequency sti

84 vels and selectively blocks the induction of long-term potentiation in striatal cholinergic interneur

85 nt deficit in the maintenance of hippocampal long-term potentiation in Sumo2 knockout mice.

86 naptic transmission in the dentate gyrus and long-term potentiation in the CA1 region of the hippocam

87 Traumatic brain injury reduced long-term potentiation in the hippocampal slices, and L-

88 tion, because traumatic brain injury reduces long-term potentiation in the hippocampus, a cellular co

89 fast excitatory transmission and facilitates long-term potentiation in the hippocampus, two effects l

90 At the physiological level, TBI suppressed long-term potentiation in the hippocampus, which was ful

91 affected neuronal plasticity by facilitating long-term potentiation in the hippocampus.

92 ted mGlu5 receptor-dependent facilitation of long-term potentiation in the IL-PFC.

93 probability of LTD without affecting that of long-term potentiation in the insular cortex.

94 ts in object recognition memory and impaired long-term potentiation in the prefrontal cortex.

95 rea CA1 depotentiates previously established long-term potentiation in the Schaffer collateral (SC) p

96 f-administration, similar to cocaine-induced long-term potentiation in the VTA.

97 age-dependent reduction in spine density and long-term potentiation in their hippocampus.

98 ity, leads to a complete block of subsequent long-term potentiation induction and a facilitation of l

99 We have shown that PPZ restores long-term potentiation induction in 6-month-old 5xFAD mo

100 jection, both domain-specific mAbs abrogated long-term potentiation induction, and LRR-directed antib

101 otine and NRG3 facilitated the conversion of long-term potentiation into long-term depression at cort

102 knocked out (MKP-2(-/-) mice), we show that long-term potentiation is impaired in MKP-2(-/-) mice co

103 bound depolarization, and non-mGluR-mediated long-term potentiation is unaltered.

104 ayed impaired cognition and hippocampal late long-term potentiation (L-LTP).

105 lteration of synaptic strength necessary for long-term potentiation, learning, and memory.

106 Intracortical facilitation and long-term potentiation-like plasticity were impaired in

107 tly reduced and the resulting suppression of long term potentiation (LTP) by Abeta oligomers was prev

108 ic GluN2A-containing NMDARs and induction of long term potentiation (LTP) lead to the translocation o

109 rtant role in learning and memory as well as long term potentiation (LTP).

110 atio of AMPAR EPSCs and elevated early-phase long term potentiation (LTP).

111 ing and Rac1 expression, spatial memory, and long-term potentiation (LTP) abnormalities in adult mice

112 mbers (APP, APLP1, APLP2), develop defective long-term potentiation (LTP) and aged mice display spati

113 memantine-induced enhancement of hippocampal long-term potentiation (LTP) and CaMKII activity was tot

114 Long-term potentiation (LTP) and depression (LTD) at glu

115 facilitate the induction of Hebbian forms of long-term potentiation (LTP) and depression (LTD) by aff

116 Both long-term potentiation (LTP) and depression (LTD) of exc

117 Hebbian plasticity, comprised of long-term potentiation (LTP) and depression (LTD), allow

118 ive GSK3beta caused a significant deficit in long-term potentiation (LTP) and facilitated long-term d

119 displayed significantly enhanced hippocampal long-term potentiation (LTP) and increased dendritic spi

120 activation is required for the induction of long-term potentiation (LTP) and is generally neuroprote

121 At glutamatergic synapses, both long-term potentiation (LTP) and long-term depression (L

122 wn to support such bidirectional changes are long-term potentiation (LTP) and long-term depression (L

123 lutamate receptors (NMDAR, AMPAR), including long-term potentiation (LTP) and long-term depression (L

124 xemplified by the enhancement of hippocampal long-term potentiation (LTP) and long-term depression (L

125 l synaptic plasticity has largely focused on long-term potentiation (LTP) and long-term depression (L

126 essary and sufficient for the maintenance of long-term potentiation (LTP) and long-term memory (LTM).

127 intermediate strength level from which both long-term potentiation (LTP) and LTD are possible.

128 but not monomers, produces an impairment of long-term potentiation (LTP) and memory, independent of

129 nt concentrations of Abeta are necessary for long-term potentiation (LTP) and memory.

130 ant synaptic protein CaMKII is necessary for long-term potentiation (LTP) and memory.

131 de in the healthy brain, enhance hippocampal long-term potentiation (LTP) and memory.

132 centrations, the peptide is needed to ensure long-term potentiation (LTP) and memory.

133 owth factor-like properties and can modulate long-term potentiation (LTP) and memory.

134 stimulation is accompanied by impairment in long-term potentiation (LTP) and spatial learning.

135 ns increased ERK signaling and impaired both long-term potentiation (LTP) and spatial memory in mice,

136 SIGNIFICANCE STATEMENT: Various types of long-term potentiation (LTP) are correlated with distinc

137 odic memory, and synaptic changes induced by long-term potentiation (LTP) are thought to underlie mem

138 e, we show that this procedure also leads to long-term potentiation (LTP) at an excitatory synapse, d

139 Deficits in long-term potentiation (LTP) at central excitatory synap

140 nhances - not antagonizes - the induction of long-term potentiation (LTP) at excitatory, axospinous s

141 al injury relaxes the timing rules governing long-term potentiation (LTP) at mouse primary afferent s

142 re-NMDARs also control the dynamic range for long-term potentiation (LTP) at MPP-GC synapses, an effe

143 Long-term potentiation (LTP) at parallel fiber (PF)-Purk

144 p.) impaired short-term plasticity (STP) and long-term potentiation (LTP) at perforant path-DG synaps

145 synaptic and postsynaptic activity can evoke long-term potentiation (LTP) at sensory synapses onto ad

146 arbors and spines as well as a reduction in long-term potentiation (LTP) at the associational-commis

147 deed, genetic deletion of Calstabin2 reduced long-term potentiation (LTP) at the hippocampal CA3-CA1

148 Several forms of long-term potentiation (LTP) at the Schaffer collateral

149 Long-term potentiation (LTP) at the Schaffer collateral-

150 nd reduced the NMDAR synaptic potentials and long-term potentiation (LTP) at the Schaffer collaterals

151 Remarkably, long-term potentiation (LTP) can override the masking ef

152 Aged mice displayed a CA1 long-term potentiation (LTP) deficit that was not associ

153 creased inducibility of associative synaptic long-term potentiation (LTP) due to saturation after sle

154 t calpain-1 is required for the induction of long-term potentiation (LTP) elicited by theta-burst sti

155 The synapse specificity of long-term potentiation (LTP) ensures that no interferenc

156 onstrate that TBI inhibits the expression of long-term potentiation (LTP) evoked by high-frequency st

157 and improved memory deficits and hippocampal long-term potentiation (LTP) impairments without alterin

158 Since the discovery of long-term potentiation (LTP) in 1973, thousands of paper

159 Here, we show that sAPPalpha facilitates long-term potentiation (LTP) in a concentration-dependen

160 tinence and observed an increase in moderate long-term potentiation (LTP) in cocaine-treated rats com

161 nsistent with previous studies, we show that long-term potentiation (LTP) in cortico-striatal circuit

162 ors (betaARs) enhances both the induction of long-term potentiation (LTP) in hippocampal CA1 pyramida

163 exity, increased spine density, and enhanced long-term potentiation (LTP) in hippocampal neurons.

164 stores theta burst stimulation (TBS)-induced long-term potentiation (LTP) in hippocampal slices from

165 ABSTRACT: NMDA receptor independent long-term potentiation (LTP) in hippocampal stratum orie

166 imulation of corticostriatal fibres produces long-term potentiation (LTP) in striatal projection neur

167 hannels completely suppressed development of long-term potentiation (LTP) in the CA1-subiculum, but n

168 soform, completely suppressed development of long-term potentiation (LTP) in the CA1-subiculum, but n

169 In this study, long-term potentiation (LTP) in the CNS of the medicinal

170 g-dependent long-term depression switches to long-term potentiation (LTP) in the former, timing-depen

171 Electrophysiology experiments showed that long-term potentiation (LTP) in the hippocampus, which i

172 Although long-term potentiation (LTP) in the lateral amygdala (LA

173 Long-term potentiation (LTP) in the rat hippocampus is t

174 r-weight MAP2 in vivo abolished induction of long-term potentiation (LTP) in the Schaffer collateral

175 l adipose NLRP3 was required for deficits in long-term potentiation (LTP) in transplant recipients, a

176 Long-term potentiation (LTP) is a rapid and persistent i

177 Long-term potentiation (LTP) is an activity-dependent an

178 Long-term potentiation (LTP) is widely perceived as a me

179 itutively repress the expression of synaptic long-term potentiation (LTP) of C-fiber-evoked potential

180 imulation (LFS) to the sciatic nerve induced long-term potentiation (LTP) of C-fiber-evoked potential

181 amate receptor type 1 (mGluR1)-mediated late long-term potentiation (LTP) of excitatory input synapse

182 Long-term potentiation (LTP) of excitatory synaptic tran

183 s of drug addiction indicate that persistent long-term potentiation (LTP) of excitatory synaptic tran

184 of the rodent hippocampus exhibit a form of long-term potentiation (LTP) of glutamatergic transmissi

185 Long-term potentiation (LTP) of mature neurons produces

186 n patterns reliably elicited a novel form of long-term potentiation (LTP) of MNTB-LSO synapses.

187 We found that long-term potentiation (LTP) of mossy fiber input invoke

188 nsive analysis of APA following induction of long-term potentiation (LTP) of mouse hippocampal CA3-CA

189 Long-term potentiation (LTP) of NMDA receptor (NMDAR)-me

190 ess in rats causes persistent enhancement of long-term potentiation (LTP) of NMDA receptor-mediated g

191 Mossy fiber input is known to exhibit a long-term potentiation (LTP) of synaptic efficacy throug

192 d odor exposure, induces glomerulus-specific long-term potentiation (LTP) of synaptic strength select

193 and cognition are thought to require normal long-term potentiation (LTP) of synaptic strength, which

194 Surprisingly, we find that long-term potentiation (LTP) of synaptic transmission at

195 in (CaN) both bind open calmodulin, favoring Long-Term Potentiation (LTP) or Depression (LTD) respect

196 ed in the hippocampus following induction of long-term potentiation (LTP) or learning.

197 of the neuronal synapse, phenomena known as long-term potentiation (LTP) or long-term depression (LT

198 Cortical plasticity mechanisms of long-term potentiation (LTP) or of long-term depression

199 eby AMPARs are inserted into synapses during long-term potentiation (LTP) or removed during long-term

200 atum has been characterized, their effect on long-term potentiation (LTP) remains unknown.

201 Long-lasting forms of long-term potentiation (LTP) represent one of the major

202 DA (N-methyl-d-aspartate) receptor-dependent long-term potentiation (LTP) shapes neural circuits and

203 ly more mushroom spines and higher-magnitude long-term potentiation (LTP) than SR synapses.

204 esynaptic, NMDA-receptor-independent form of long-term potentiation (LTP) that requires postsynaptic

205 Whereas the presynaptic form of mossy fiber long-term potentiation (LTP) was not affected, the posts

206 ory molecule, even before its involvement in long-term potentiation (LTP) was shown.

207 directionally modified through potentiation (long-term potentiation (LTP)) or depression (long-term d

208 endotoxemia experienced loss of hippocampal long-term potentiation (LTP), a brain-derived neurotroph

209 ual fear memory and increase the duration of long-term potentiation (LTP), a form of hippocampal syna

210 n is an essential step for the expression of long-term potentiation (LTP), a long-lasting, activity-d

211 ampal CA3 and CA1 pyramidal neurons exhibits long-term potentiation (LTP), a positive feedback proces

212 lasting changes in synaptic strength such as long-term potentiation (LTP), a putative cellular mechan

213 Long-term potentiation (LTP), an increase in synaptic ef

214 show impaired NMD, memory deficits, abnormal long-term potentiation (LTP), and social and communicati

215 dendritic integration of excitatory inputs, long-term potentiation (LTP), and spatial memory formati

216 put specificity is a fundamental property of long-term potentiation (LTP), but it is not known if lea

217 models demonstrated exaggerated hippocampal long-term potentiation (LTP), consistent with deficits i

218 used to monitor synaptic strength and induce long-term potentiation (LTP), does not exclusively recru

219 emory and its electrophysiological surrogate long-term potentiation (LTP), effects that may be mediat

220 Ex vivo, OF enabled induction of long-term potentiation (LTP), expressed mostly postsynap

221 We show that long-term potentiation (LTP), in the CA1 region of hippo

222 Biological synaptic behaviors such as long-term potentiation (LTP), long-term depression (LTD)

223 -aspartate (NMDA) receptor (NMDAR)-dependent long-term potentiation (LTP), remains unclear.

224 One is the discovery of long-term potentiation (LTP), the phenomenon that brief,

225 that a classical synaptic memory mechanism, long-term potentiation (LTP), triggers withdrawal of PAP

226 ts, wash-in of letrozole virtually abolished long-term potentiation (LTP), whereas it did not prevent

227 ments is most likely mediated by fast-acting long-term potentiation (LTP), which relies on the precis

228 ive stimulation, which is thought to reflect long-term potentiation (LTP)-like cortical plasticity (n

229 CS-LTD in superficial cortical layers, and a long-term potentiation (LTP)-like enhancement (DCS-LTP)

230 MS-theta burst stimulation was used to probe long-term potentiation (LTP)-like plasticity in M1.

231 ss of neuronal functions, including synaptic long-term potentiation (LTP).

232 rol involved in long-term memory and in late long-term potentiation (LTP).

233 the synapse, but was incapable of expressing long-term potentiation (LTP).

234 ngth by facilitating an anti-Hebbian form of long-term potentiation (LTP).

235 aptic plasticity loss evident by a decreased long-term potentiation (LTP).

236 aptic transmission and are unable to sustain long-term potentiation (LTP).

237 ction of both long-term depression (LTD) and long-term potentiation (LTP).

238 nd ablates Reelin stimulation of hippocampal long-term potentiation (LTP).

239 ecessary and sufficient for the induction of long-term potentiation (LTP).

240 thesis required to sustain the late phase of long-term potentiation (LTP).

241 memory impairments, we examined hippocampal long-term potentiation (LTP).

242 ally reduces basal synaptic transmission and long-term potentiation (LTP).

243 ethyl-d-aspartate receptor (NMDAR)-dependent long-term potentiation (LTP).

244 riments examining the effects on hippocampal long-term potentiation (LTP).

245 icantly enriched in proteins associated with long-term potentiation (LTP).

246 lular processes underlying learning, such as long-term potentiation (LTP).

247 ted memory deficits and impaired hippocampal long-term potentiation (LTP).

248 plasmic equilibrium, and capacity to inhibit long-term potentiation (LTP).

249 plasticity, as evidenced by greatly enhanced long-term potentiation (LTP).

250 paired-pulse facilitation, IH(30) suppressed long-term potentiation (LTP).

251 embrane electrophysiological properties, and long-term potentiation (LTP).

252 ), or patterns of synaptic activation, as in long-term potentiation (LTP).

253 D and FBD pathogenesis by impairing synaptic Long-term potentiation (LTP).

254 ouse model of Alzheimer's disease (AD), late long-term potentiation (LTP; L-LTP) and its associative

255 epression (LTD) of synaptic transmission but long-term-potentiation (LTP) of synaptic signals in HIL

256 d glutamatergic transmission, suppression of Long-term-Potentiation (LTP), an electrophysiological su

257 Synaptic plasticity (e.g., long-term potentiation [LTP]) is considered the cellular

258 erosynaptic and is expressed as an increase (long-term potentiation, LTPGABA) or a decrease (long-ter

259 is not the case for hippocampal presynaptic long-term potentiation (LTPpre), which is expressed as a

260 Long-term potentiation of excitatory synapses on pyramid

261 hippocampal stratum oriens exhibit a form of long-term potentiation of excitatory transmission that i

262 atterns of postsynaptic activity that induce long-term potentiation of fast excitatory transmission a

263 showed reduced initiation and maintenance of long-term potentiation of glutamatergic synapses.

264 eatment, lOFC neurons displayed a persistent long-term potentiation of glutamatergic synaptic transmi

265 Long-term potentiation of glutamatergic transmission to

266 ' inputs; and rapid gating input scaling via long-term potentiation of intrinsic excitability (LTP-IE

267 BCG led to short-term and long-term potentiation of monocyte-derived cytokine resp

268 al area CA1 heterosynaptically depotentiates long-term potentiation of Schaffer collateral (SC) synap

269 However, long-term potentiation of the temporoammonic pathway to

270 on network where memristive synapses undergo long-term potentiation or depression driven by neuronal

271 of the neurons, basal synaptic transmission, long-term potentiation or expression of LTD.

272 of Mef2c did not impact learning and memory, long-term potentiation, or social and repetitive behavio

273 e in adult brain involved genes enriched for long-term potentiation pathways.

274 ffects combined with PE-induced anti-Hebbian long-term potentiation reported in a previous study coul

275 epression (required for Dc-ODP), and CREB in long-term potentiation (required for Pc-ODP).SIGNIFICANC

276 avage, ameliorates synapse loss and augments long-term potentiation, resulting in protection of memor

277 in single dendritic spines during structural long-term potentiation (sLTP) in hippocampal CA1 pyramid

278 escribe a three-molecule model of structural long-term potentiation (sLTP) of murine dendritic spines

279 of neuronal plasticity, including structural long-term potentiation (sLTP), which is a correlate of a

280 inhibits microglial activation and enhances long-term potentiation, synaptic plasticity, neurogenesi

281 exclusively produced spike timing-dependent long-term potentiation (t-LTP) in projection neurons pre

282 undergone theta-burst stimulation to produce long-term potentiation (TBS-LTP) and compared them to co

283 imilar to the memory deficits, theta-induced long-term potentiation (theta-LTP) in the nucleus accumb

284 esulted in the conversion of early into late long-term potentiation through the nitric oxide/cGMP/pro

285 n hyperexcitability and impaired hippocampal long-term potentiation, through a monosynaptic LH(GABA)

286 n naive male mice, to spike-timing-dependent long-term potentiation (tLTP) in DID mice, an effect tha

287 e role of GSK3beta in spike timing-dependent long-term potentiation (tLTP) in the chronic unpredictab

288 ber synapses in area CA3 and found increased long-term potentiation upon depletion of IFT20 or disrup

289 Synaptic long-term potentiation was abolished following intracere

290 Hippocampal long-term potentiation was decreased in both chronic BAC

291 tly different between the two MA groups, but long-term potentiation was greater in ampakine-treated r

292 More importantly, hippocampal CA1 long-term potentiation was markedly impaired in parabiot

293 red 1 week after traumatic brain injury, and long-term potentiation was studied using field recording

294 ence and magnitude of spike timing-dependent long-term potentiation were significantly higher at musc

295 ed with confocal microscopy) and plasticity (long-term potentiation) were examined in the hippocampus

296 pathogenic effects (memory, synaptic NMDAR, long-term potentiation) were prevented in the animals tr

297 This potentiation occludes long-term potentiation, which could be rescued, to some

298 fusion lead to CaMKII activation and calcium long-term potentiation, which support cardiomyocyte cont

299 water maze, and a significant disruption of long-term potentiation without alteration of long-term d

300 e tolerance, OIH and pronociceptive synaptic long-term potentiation without altering antinociception.