ライフサイエンスコーパス: long-term depression

1 is, a process important in the expression of long term depression.

2 d reduced the susceptibility to induction of long-term depression.

3 AR)-induced AMPAR endocytosis and cerebellar long-term depression.

4 naptic plasticity in the cerebellum, such as long-term depression.

5 rough a postsynaptic mechanism, and disrupts long-term depression.

6 little effect on decreased AMPAR levels with long-term depression.

7 es cognitive function in rodents by blocking long-term depression.

8 with antibodies prevents the facilitation of long-term depression.

9 Reversing the timing of the inputs induced long-term depression.

10 ration of supralinear Ca2+ events, triggered long-term depression.

11 including an NMDA receptor-dependent form of long-term depression.

12 pses onto hippocampal CA1 neurons to undergo long-term depression.

13 iation was also increased, with no change in long-term depression.

14 hreshold induction stimuli, without altering long-term depression.

15 ificantly reduced long-term potentiation and long-term depression.

16 sed in Purkinje cells, eliminates cerebellar long-term depression.

17 larger long-term potentiation, and deficient long-term depression.

18 panied by impaired endocannabinoid-dependent long-term depression.

19 cades, leading to long-term potentiation and long-term depression.

20 efrontal cortex undergoing robust HA-induced long-term depression.

21 ncement of the GSK3beta activity and thereby long-term depression.

22 taplastic upregulation of oxytocin-dependent long-term depression.

23 complex spikes do not induce parallel fibre long-term depression.

24 uning, internalization of AMPA receptors and long-term depression.

25 mpal neurons abolishes NMDA-induced chemical long-term depression.

26 y in neurons in response to the induction of long-term depression.

27 SSRIs selectively inhibited hippocampal long-term depression.

28 down-regulation evoked by chemically induced long-term depression.

29 spartate currents and the ability to exhibit long-term depression.

30 y during chemical long-term potentiation and long-term depression.

31 presynaptic NMDARs, and promotes presynaptic long-term depression.

32 sive enzymes in processes including synaptic long-term depression.

33 zation, 32 of 76 regular inputs (42%) showed long-term depression, 21 inputs (28%) showed potentiatio

34 was associated with enhanced mGluR-mediated long-term depression, a form of synaptic plasticity.

35 Long-term depression, a proposed physiological correlate

36 n pyramidal neurons correlated with enhanced long-term depression and blunted depotentiation of long-

37 The Deltap35KI mice exhibit impaired long-term depression and defective memory extinction, li

38 et1KO animals exhibited abnormal hippocampal long-term depression and impaired memory extinction.

39 genetic removal of presynaptic D2Rs impaired long-term depression and performances on spatial memory

40 the synaptic modification threshold between long-term depression and potentiation in pyramidal neuro

41 somatostatin expressing interneurons undergo long-term depression and potentiation respectively (PV-i

42 The maternal effects on both long-term depression and PPD were eliminated by treatmen

43 ss, impairs long-term potentiation, enhances long-term depression, and induces learning and memory de

44 ckdown (KD) in vivo blocks this LTP, but not long-term depression, and reduces frequencies of miniatu

45 nt in long-term potentiation, enhancement in long-term depression, and weakened spatial memory, these

46 derived neurotrophic factor (BDNF) to induce long-term depression, and with the BDNF receptor tyrosin

47 tly, we find that long-term potentiation and long-term depression are independently modulated with le

48 , long-term potentiation and mGluR-dependent long-term depression are normal at CA3-CA1 pyramidal cel

49 otropic glutamate receptor (mGluR)-dependent long-term depression, are dysregulated at medial perfora

50 (metabotropic glutamate receptor)-dependent long-term depression, as well as for other forms of syna

51 Canonical JAK-STAT signaling is pivotal for long-term depression at adult hippocampal temporoammonic

52 he conversion of long-term potentiation into long-term depression at cortical layer 3/5 synapses.

53 s down-regulated, and CB1 receptor-dependent long-term depression at DLS synapses was absent.

54 M(1) mAChR activation induced long-term depression at inputs from the ventral hippocam

55 We describe a novel form of long-term depression at parvalbumin-expressing (PV+) int

56 term potentiation and facilitated subsequent long-term depression at synapses quiescent during primin

57 bthalamic nucleus neurons and in measures of long-term depression at the hippocampal Schaffer collate

58 leads to NMDA receptor- and Ca(2+)-dependent long-term depression at these synapses.

59 induction of long-term potentiation, but not long-term depression, at the synapses between the entorh

60 ) mice in the alterations in mGluR-dependent long-term depression, basal protein synthesis, and dendr

61 electrically induced and chemically induced long-term depression, but not long-term potentiation, in

62 nce thalamocortical transmission and inhibit long-term depression by mechanistically distinct presyna

63 Induction of long-term depression by nicotine relied on nicotinic rec

64 acute immobilization stress attenuates this long-term depression by recruiting endogenous H(3) recep

65 The inhibition of long-term depression by SSRIs was mediated by a direct b

66 a-catenin stabilization was found to abolish long-term depression by stabilizing cadherin at the syna

67 he theory predicts presynaptic expression of long-term depression, consistent with experimental obser

68 oss of Gprasp2 leads to enhanced hippocampal long-term depression, consistent with facilitated mGluR-

69 Cathodal DCS in vitro induces a long-term depression (DCS-LTD) of excitatory synaptic st

70 ectopic release pools by activity-dependent long-term depression decreased EPSC decay time, revealin

71 of an endocannabinoid (eCB)-mediated form of long-term depression (eCB-LTD) at adult central glutamat

72 -nociceptive afferents elicits eCB-dependent long-term depression (eCB-LTD) heterosynaptically in noc

73 the effect of PE on endocannabinoid-mediated long-term depression (eCB-LTD) in VTA DA neurons.

74 Endocannabinoid-dependent long-term depression (eCB-LTD) is the best characterized

75 Retrograde endocannabinoid-mediated long-term depression (eCB-LTD) was ablated in mBACtgDyrk

76 moderate levels of eCB lead to eCB-mediated long-term depression (eCB-tLTD) while short and large eC

77 is heterosynaptic, endocannabinoid-dependent long-term depression (ecLTD) is observed where the T- an

78 haffer collateral-CA1 neurons was normal but long-term depression evoked by paired-pulse low-frequenc

79 of the temporal hippocampus tightly modulate long-term depression expression and play a major role in

80 nhibition is highly plastic, and undergoes a long-term depression following high-frequency 10 Hz or t

81 entials from the lateral dorsal thalamus and long-term depression following tetanization of this inpu

82 roactive ligand-receptor interaction and the long-term depression gene set.

83 synaptic currents (IPSCs) followed by modest long-term depression (I-LTD) in dopamine neurons of rat

84 s of the rat somatosensory nucleus develop a long-term depression (I-LTD) when challenged by a stimul

85 type glutamate receptor (NMDAR)-induction of long term depression in the CA1 region of the hippocampu

86 e capable of undergoing experience-dependent long-term depression in a voltage- and eCB-dependent man

87 synthesis and an increase in mGluR-dependent long-term depression in CA1 of the hippocampus that is i

88 creased long-term potentiation and decreased long-term depression in corticostriatal synapses.

89 tive allosteric modulator, which facilitates long-term depression in direct pathway neurons and rever

90 neurons predominantly evoked NMDAR-dependent long-term depression in naive Gad67-GFP interneurons.

91 nhibitor-2 was critical for the induction of long-term depression in primary neurons.

92 Though the role of opioid receptors in long-term depression in striatum has been characterized,

93 showed increased hippocampal mGluR1-induced long-term depression in the adult offspring of high-LG c

94 lization of AMPARs and for the expression of long-term depression in the cerebellum.

95 iation using the same protocol that elicited long-term depression in the dorsolateral striatum.

96 metabotropic glutamate receptor-5-dependent long-term depression in the hippocampus and cerebellum.

97 sion correlates with attenuated DHPG-induced long-term depression in the hippocampus of RS model mice

98 we found that activation of mGlu3 can induce long-term depression in the mouse medial PFC (mPFC) in v

99 well as deficits in NMDA receptor-dependent long-term depression in the nucleus accumbens core after

100 linked to deficits in the ability to induce long-term depression in the nucleus accumbens, as well a

101 rm object recognition memory and facilitates long-term depression in the perirhinal cortex, a neural

102 nic acetylcholine receptor (mAChR)-dependent long-term depression in the PFC that we hypothesize is i

103 ne modulated both long-term potentiation and long-term depression in the temporal hippocampus as well

104 N-methyl-d-aspartic acid receptor-dependent long-term depression in these mice, which could be norma

105 (NMDAR)-dependent long-term potentiation and long-term depression in USP6 transgenic mouse hippocampi

106 rsive, and low-frequency stimulation induces long-term depression in vitro.

107 ating 2-arachidonoylglycerol levels restored long-term depression in YAC128 striatal neurons.

108 on of oxytocin-mediated synaptic plasticity (long-term depression) in the nucleus accumbens establish

109 these treatments did not affect hippocampal long-term depression induced by low frequency electrical

110 potentiation induction and a facilitation of long-term depression induction in neurons expressing chi

111 could be rescued, to some extent, with prior long-term depression induction.

112 Long-term potentiation is abolished and long-term depression is enhanced in the hippocampus, and

113 epolarization-induced calcium rises, whereas long-term depression is induced by synaptic activation o

114 This long-term depression is postsynaptically expressed, trop

115 NAc transmission by optogenetic induction of long-term depression is pro-resilient, whereas acute enh

116 Making a long term depression-like plastic change to dIPL node tr

117 lobule (dIPL)-M1 before and after inducing a long term depression-like plastic change to dIPL node wi

118 receptors in BNST VGAT neurons can induce a long-term depression-like state of glutamatergic synapti

119 Long-term depression (LTD) (selective weakening of speci

120 tion, the responses of MeA neurons underwent long-term depression (LTD) after theta burst stimulation

121 , including long-term potentiation (LTP) and long-term depression (LTD) and homeostatic scaling.

122 aminergic modulation of both corticostriatal long-term depression (LTD) and long-term potentiation (L

123 recordings were used to determine changes in long-term depression (LTD) and long-term potentiation (L

124 ocampal synaptic plasticity, specifically in long-term depression (LTD) and long-term potentiation (L

125 tion that lead to impaired induction of both long-term depression (LTD) and long-term potentiation (L

126 ARs) as a key target for synaptic removal in long-term depression (LTD) and persistent fear attenuati

127 sphorylation that simulates the induction of long-term depression (LTD) and potentiation (LTP) at the

128 slices, we show that MD selectively induces long-term depression (LTD) and shifts spike timing-depen

129 aviors such as long-term potentiation (LTP), long-term depression (LTD) and spike-timing dependent pl

130 Long-term potentiation (LTP) and long-term depression (LTD) are key mechanisms of synapti

131 Long-term potentiation (LTP) and long-term depression (LTD) are the two major forms of lo

132 de of BLA-GC synaptic responses, pointing to long-term depression (LTD) as a mechanism for learning.

133 We show that long-term depression (LTD) at corticostriatal synapses o

134 by a single presynaptic spike induces robust long-term depression (LTD) at developing layer 4 to laye

135 DA receptor and protein kinase C-independent long-term depression (LTD) at hippocampal CA3-CA1 synaps

136 role for this pathway in activity-dependent long-term depression (LTD) at hippocampal Schaffer colla

137 ere we identify a crucial role for ASIC1a in long-term depression (LTD) at mouse insular synapses.

138 e learning mechanism in conditioning is that long-term depression (LTD) at parallel fiber (PF)-Purkin

139 acquisition of the conditioned response: (1) long-term depression (LTD) at parallel fiber-Purkinje ce

140 ative cellular mechanism for motor learning, long-term depression (LTD) at parallel fibre-Purkinje ce

141 Furthermore, BDNF/TrkB signaling mediated long-term depression (LTD) at postsynaptic sites in ovBN

142 In long-term depression (LTD) at synapses in the adult brai

143 Long-term depression (LTD) at these synapses is driven b

144 Long-term depression (LTD) between cortical layer 4 spin

145 P including long-term potentiation (LTP) and long-term depression (LTD) can be induced at GABAergic s

146 apses, both long-term potentiation (LTP) and long-term depression (LTD) can be induced at the same sy

147 h LTP in vivo facilitates, while optogenetic long-term depression (LTD) diminishes, the behavioral ef

148 in another type of synaptic plasticity, the long-term depression (LTD) elicited by activation of typ

149 In contrast, long-term depression (LTD) emerges in the absence of PII

150 ation of adenosine A1 receptors prevents the long-term depression (LTD) evoked in the somatosensory c

151 amp experiments from Nacc slices reveal that long-term depression (LTD) formation is hampered, with p

152 exposure to dopamine can restore the loss of long-term depression (LTD) formation, counteract the red

153 changes are long-term potentiation (LTP) and long-term depression (LTD) forms that relay on the activ

154 mate receptor (mGluR)-dependent homosynaptic long-term depression (LTD) has been studied extensively

155 by inducing long-term potentiation (LTP) and long-term depression (LTD) in anesthetized mice in vivo.

156 The expression of long-term depression (LTD) in cerebellar Purkinje cells

157 chanisms of long-term potentiation (LTP) and long-term depression (LTD) in other brain regions.

158 long-term potentiation (LTP) and facilitated long-term depression (LTD) in PFC pyramidal neurons.

159 chanisms of long-term potentiation (LTP) and long-term depression (LTD) in principal neurons of the b

160 n (LTP) in wild-type (WT) animals, it caused long-term depression (LTD) in Prnp(0/0) mice.

161 changes of long-term potentiation (LTP) and long-term depression (LTD) in response to fluctuations i

162 Here we show that long-term depression (LTD) in the area CA1 of neonatal r

163 ss this question for NMDA receptor-dependent long-term depression (LTD) in the hippocampus.

164 ecessary for the induction of M(1)-dependent long-term depression (LTD) in the prefrontal cortex (PFC

165 or antagonist CTAP, suggesting an inhibitory long-term depression (LTD) induced by an exogenous mu-op

166 Upon redistribution of Inp54p, long-term depression (LTD) induced by low-frequency stim

167 ale mice trigger metaplastic facilitation of long-term depression (LTD) induction at hippocampal CA1

168 y stimulus electrophysiological paradigm for long-term depression (LTD) induction, we examined the ro

169 , long-term potentiation (LTP) is intact but long-term depression (LTD) is impaired in K(b)D(b)(-/-)

170 interplay between long-term potentiation and long-term depression (LTD) is thought to be involved in

171 as demonstrated an increased mGluR5-mediated long-term depression (LTD) leading to several clinical t

172 focused on long-term potentiation (LTP) and long-term depression (LTD) mechanisms that rely on the a

173 stimulation (HFS) of cortical inputs induced long-term depression (LTD) mediated by adenosine A1 rece

174 application suppresses the induction of the long-term depression (LTD) normally caused by pairing 10

175 Long-term depression (LTD) of excitatory synaptic transm

176 an affect neuronal communication by inducing long-term depression (LTD) of excitatory transmission at

177 ow report that activation of mGlu(3) induces long-term depression (LTD) of excitatory transmission in

178 now report that activation of mGlu3 induces long-term depression (LTD) of excitatory transmission in

179 in the ventral tegmental area (VTA) induces long-term depression (LTD) of GABAergic synapses on DA n

180 of alpha1-ARs induced an inward current and long-term depression (LTD) of glutamate synapses of DRn

181 ning leads to dopamine receptor D4-dependent long-term depression (LTD) of glutamatergic excitatory s

182 2-like receptors (D2Rs) leads selectively to long-term depression (LTD) of hippocampal-PFC NMDAR-medi

183 Presynaptic long-term depression (LTD) of synapse efficacy generally

184 amate receptors (NMDARs) in conjunction with long-term depression (LTD) of synaptic strength.

185 rols long-term potentiation (LTP) as well as long-term depression (LTD) of synaptic transmission, cel

186 curs via mechanisms revealed by the study of long-term depression (LTD) of synaptic transmission, whi

187 Long-term depression (LTD) of the efficacy of synaptic t

188 NR2A expression did not affect 1-Hz-induced long-term depression (LTD) or 100 Hz-induced long-term p

189 (TEPs) changed differently according to the long-term depression (LTD) or potentiation (LTP) after-e

190 Conversely, long-term depression (LTD) promoted ADAM10 synaptic memb

191 rapid forms of AMPAR internalization during long-term depression (LTD) require clathrin and dynamin,

192 gnitudes of long-term potentiation (LTP) and long-term depression (LTD) to assess deficits in bidirec

193 a 1 h restraint stress induced a switch from long-term depression (LTD) to long-term potentiation (LT

194 cocaine withdrawal, in vivo circuit-specific long-term depression (LTD) unmasks the therapeutic power

195 ase kinase-3beta (GSK-3beta) is required for long-term depression (LTD) via molecular mechanisms that

196 assessed whether BNST group I mGluR-mediated long-term depression (LTD) was disrupted at these timepo

197 This long-term depression (LTD) was mediated by the endocanna

198 her potentiate these maxed-out synapses, but long-term depression (LTD) was readily induced by low-fr

199 Reduced long-term depression (LTD) was recently reported in TSC

200 Long-term depression (LTD) weakens synaptic transmission

201 anisms of long-term potentiation (LTP) or of long-term depression (LTD) were assessed using respectiv

202 long-term potentiation (LTP)) or depression (long-term depression (LTD)) as well as the phosphorylati

203 to AMPA receptor (AMPAR) internalization and long-term depression (LTD), although the signaling pathw

204 anced long-term potentiation (LTP), impaired long-term depression (LTD), and a thinning of the postsy

205 hippocampal long-term potentiation (LTP) and long-term depression (LTD), and for the regulation of th

206 Its neuronal functions now extend to long-term depression (LTD), and last year saw the first

207 ing this subunit have a critical role in pRh long-term depression (LTD), one of the primary physiolog

208 apses during long-term potentiation (LTP) or long-term depression (LTD), or globally during homeostat

209 ena known as long-term potentiation (LTP) or long-term depression (LTD), respectively.

210 otropic glutamate receptors (mGluRs) induces long-term depression (LTD), which requires new protein s

211 exposed mice, through glutamatergic synaptic long-term depression (LTD), without significant effects

212 plasticity-long-term potentiation (LTP) and long-term depression (LTD)-have been well studied and ar

213 ves, as well as long-term potentiation (LTP)/long-term depression (LTD)-like plasticity with paired-a

214 al direct current stimulation (cDCS) induces long-term depression (LTD)-like reduction of cortical ex

215 ing in the cerebellum--which may result from long-term depression (LTD)-related disinhibition of chol

216 tex (PFC) and also display impaired cortical long-term depression (LTD).

217 ining or by optogenetic induction of in vivo long-term depression (LTD).

218 interneurons exhibit robust activity-induced long-term depression (LTD).

219 ng-term potentiation (LTP) or removed during long-term depression (LTD).

220 , including long-term potentiation (LTP) and long-term depression (LTD).

221 anisms like long-term potentiation (LTP) and long-term depression (LTD).

222 (2+) have a crucial role in the induction of long-term depression (LTD).

223 sms such as long-term potentiation (LTP) and long-term depression (LTD).

224 transmission, paired-pulse facilitation and long-term depression (LTD).

225 move synaptic and extrasynaptic GluA1 during long-term depression (LTD).

226 requency stimulation-induced NMDAR-dependent long-term depression (LTD).

227 Interestingly, late long-term depression (LTD; L-LTD) was not compromised, b

228 Augmented hippocampal mGluR-induced long-term depression (LTD; or chemically induced mGluR-L

229 g-term potentiation, LTPGABA) or a decrease (long-term depression, LTDGABA) of neurotransmitter relea

230 ate the status of long-term potentiation and long-term depression (LTP and LTD) in the associative/co

231 long-term potentiation without alteration of long-term depression, measured in ex vivo hippocampal sl

232 synapses, while another form of presynaptic long-term depression mediated by the metabotropic glutam

233 High-frequency stimulation-induced long-term depression, mediated by the endocannabinoid an

234 cal analysis reveals enhanced mGluR-mediated long-term depression (mGluR-LTD) at CA3-CA1 synapses in

235 mGluR long-term depression (mGluR-LTD) is a form of synaptic p

236 he role of NMDA receptors on mGluR-dependent long-term depression (mGluR-LTD), a key biomarker in the

237 ly, metabotropic glutamate receptor-mediated long-term depression (mGluR-LTD)-whose disruption is pos

238 ther identify N-methyl-d-aspartate-dependent long-term depression (NMDA-LTD) at prefrontal excitatory

239 NMDA receptor-dependent long-term depression (NMDAR-LTD) is a long-lasting form

240 NMDA receptor-dependent long-term depression (NMDAR-LTD), a prototypic form of s

241 However, it is unknown whether this long-term depression occurs at fear-related inputs.

242 Zhang et al. (2014) describe a novel form of long-term depression of AMPA receptor-mediated synaptic

243 ent GluD2 signaling in vivo, which underlies long-term depression of cerebellar parallel fiber-Purkin

244 ough M4 muscarinic receptors (M4Rs) promoted long-term depression of corticostriatal glutamatergic sy

245 ingly, we observed that electrically induced long-term depression of dopaminergic neurotransmission t

246 We exploited long-term depression of ectopic transmission, and select

247 activation of glutamatergic synapses drives long-term depression of electrical coupling between neur

248 otropic glutamate receptors (mGluRs) induces long-term depression of electrical synapses.

249 where it elicits a presynaptically expressed long-term depression of excitatory synaptic transmission

250 However, whereas CA1 ITDP results from long-term depression of feedforward inhibition (iLTD) as

251 Moreover, MOR-dependent long-term depression of GABA neurotransmission in the VP

252 ively couple to adenylyl cyclase to induce a long-term depression of GABA release onto both direct an

253 rotein synthesis in axon terminals to induce long-term depression of hippocampal inhibitory transmiss

254 nabinoids during the priming train to induce long-term depression of inhibition (I-LTD).

255 ing FS firing with SP depolarization induces long-term depression of inhibition at this synapse, wher

256 microcircuits, we examined voltage-dependent long-term depression of inhibitory synapses (iLTD) onto

257 ortened, and the magnitude of 2-AG-dependent long-term depression of inhibitory synapses was reduced.

258 Endocannabinoid-mediated long-term depression of inhibitory synaptic transmission

259 Here we report the discovery of long-term depression of inhibitory synaptic transmission

260 ppocampal CA1 pyramidal neurons, can trigger long-term depression of inhibitory transmission (iLTD) i

261 This long-term depression of inhibitory transmission (iLTD) i

262 s in cannabinoid-receptor 1 (CB(1))-mediated long-term depression of inhibitory transmission (iLTD),

263 cation of AM3506 to amygdala slices promoted long-term depression of inhibitory transmission, a form

264 Here we show that long-term depression of KAR-mediated synaptic transmissi

265 ion of cerebellar output mediated in-part by long-term depression of parallel fiber-Purkinje cell syn

266 lar pathway supporting an activity-dependent long-term depression of STN-SNr synapses through an NMDA

267 signalled by climbing-fibre inputs to cause long-term depression of synapses from parallel fibres to

268 Both long-term potentiation and long-term depression of synapses was dependent on postsy

269 ribe how Abeta facilitates NMDAR-independent long-term depression of synaptic transmission in the hip

270 issue of Neuron, Ma et al. (2014) show that long-term depression of two independent prefrontal corti

271 aptic plasticity, long-term potentiation and long-term depression, of excitatory synaptic transmissio

272 ed and endogenously released opioids induced long-term depression (OP-LTD) of excitatory inputs to th

273 urkinje cells is prevented without affecting long-term depression or potentiation at their parallel f

274 long-term potentiation, electrically driven long-term depression, paired pulse facilitation (PPF), s

275 were not static but became enlarged after a long-term depression paradigm.

276 thesis of proteins that lead to a functional long-term depression phenotype even when translation ini

277 metabotropic glutamate receptor 5-associated long-term depression) relevant to the pathophysiology of

278 ent increased LTP saturation levels, whereas long-term depression remained unchanged, thus leading to

279 previous reports implicating SRF and MEF2 in long-term depression (required for Dc-ODP), and CREB in

280 EN, a lipid phosphatase that is essential to long-term depression, rescued normal synaptic function a

281 al GRIP deletion was associated with blunted long-term depression, similar to what is seen following

282 While timing-dependent long-term depression switches to long-term potentiation

283 role of astrocytes in spike-timing-dependent long-term depression (t-LTD) in vivo.

284 or-dependent long-term depression, to enable long-term depression that required metabotropic glutamat

285 MSNs via presynaptic H(3) receptor-dependent long-term depression that requires G(betagamma)-directed

286 verely disrupted developmental regulation of long-term depression that we find in cortical Flailer ne

287 otropic glutamate receptor (mGluR)-dependent long-term depression that, unlike in their wild-type con

288 (preNMDAR)-mediated form of timing-dependent long-term depression (tLTD) at visual cortex layer (L) 4

289 eceptors shifted from spike-timing-dependent long-term depression (tLTD), the predominant form of pla

290 acetylcholine muscarinic receptor-dependent long-term depression, to enable long-term depression tha

291 Chemical induction of long-term depression via NMDA receptor activation causes

292 ured neurons, GluA1 synthesis after chemical long term depression was clearly diminished, and brain-d

293 Finally, long-term depression was facilitated in animals subjecte

294 g-term potentiation (LTP) and enhancement of long-term depression were corrected by the AMPK inhibito

295 1 activity is necessary for the induction of long-term depression, whereas downregulation of PP1 acti

296 ic strength and is the central mechanism for long-term depression, which underlies certain forms of l

297 ion of AMPARs and prevented the induction of long term-depression, while S-SCAM knockdown did not.

298 s in fetal brain were enriched for genes for long-term depression; while those in adult brain involve

299 Doublet stimulation is required to induce long-term depression with an optimal parallel-fibre to f

300 timulation (LFS), a protocol shown to induce long-term depression, with the aim of affecting synaptic