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

3 SSRIs selectively inhibited hippocampal long-term depression.

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

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

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

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

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

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

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

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

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

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

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

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

16 nt mechanism from long-term potentiation and long-term depression.

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

18 and that the loss of surface mGluR5 inhibits long-term depression.

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

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

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

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

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

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

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

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

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

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

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

30 Long-term depression, a proposed physiological correlate

31 mGluR- and NMDA receptor-dependent forms of long-term depression, alters the early dynamics of regul

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

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

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

35 netic deletion of KIBRA in mice impairs both long-term depression and long-term potentiation at hippo

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

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

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

39 n, but significantly impaired NMDA-dependent long-term depression and spatial learning deficits.

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

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

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

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

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

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

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

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

48 r calcium-mediated long-term potentiation or long-term depression assuming retrograde endocannabinoid

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

50 otropic glutamate receptor (mGluR)-dependent long-term depression at CA1 synapses.

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

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

53 metabotropic glutamate receptor-5-dependent long-term depression at excitatory synapses of the ventr

54 nhibition and that endocannabinoid-dependent long-term depression at inhibitory synapses (I-LTD) cons

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 egulation of both long-term potentiation and long-term depression at these synapses.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

85 potentiation and multiple distinct forms of long-term depression in adult mice.

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

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

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

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

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

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

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

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

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

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

96 NR3A is required for spike timing-dependent long-term depression in the juvenile mouse visual cortex

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

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

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

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

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

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

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

104 ed long-term potentiation (LTP) and enhanced long-term depression induced by exogenous amyloid beta p

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

106 LTP induced by high-frequency stimulation or long-term depression induced by low-frequency stimulatio

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

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

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

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

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

112 n of which can also lead to the induction of long term depression (LTD), which underlies cerebellar m

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

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

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

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

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

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

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

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

121 an intrinsic predisposition for hippocampal long-term depression (LTD) and reduced long-term potenti

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

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

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

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

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

127 thyl-d-aspartate (NMDA) receptor-independent long-term depression (LTD) at glutamate synapses of VTA

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

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

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

131 ceptors are not involved in the induction of long-term depression (LTD) at parallel fiber (PF) to Pur

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

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

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

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

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

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

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

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

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

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

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

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

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

145 e show that acute stress enables hippocampal long-term depression (LTD) in adult wild-type mice but n

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

147 e evaluated long-term potentiation (LTP) and long-term depression (LTD) in AQP4 knock-out (KO) and wi

148 were assessed at different ages in CBA mice: long-term depression (LTD) in both cerebellum and hippoc

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

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

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

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

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

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

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

156 NMDA receptor (NMDAR)-dependent long-term depression (LTD) in the hippocampus is mediate

157 We report unique evidence of long-term depression (LTD) in the juvenile songbird prem

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

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

160 Long-term depression (LTD) is an important synaptic mech

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

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

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

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

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

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

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

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

169 activates 5-HT(1b) receptors resulting in a long-term depression (LTD) of glutamate release and stri

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

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

172 t remains controversial whether they mediate long-term depression (LTD) of glutamatergic synapses ont

173 2-like receptors (D2Rs) leads selectively to long-term depression (LTD) of hippocampal-PFC NMDAR-medi

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

175 Long-term depression (LTD) of synaptic strength is an ac

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

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

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

179 ic processes such as NMDA receptor-dependent long-term depression (LTD) of synaptic transmission.

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

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

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

183 tory thalamus and cortex, we determined that long-term depression (LTD) persists at mature TC synapse

184 An NMDAR-dependent form of long-term depression (LTD) produced by low-frequency sti

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

186 underlying long-term potentiation (LTP) and long-term depression (LTD) remains poorly understood.

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

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

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

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

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

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

193 In two independent measures, however, long-term depression (LTD) was unaffected in tissue from

194 Long-term depression (LTD) weakens synaptic transmission

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

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

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

198 rupted both long-term potentiation (LTP) and long-term depression (LTD), and led to deficits in learn

199 Recent findings also implicate CaMKII in long-term depression (LTD), as well as functional roles

200 otropic glutamate receptor (mGluR)-dependent long-term depression (LTD), depend on protein translatio

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

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

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

204 uired for spine enlargement; however, during long-term depression (LTD), spines shrink via actin depo

205 botropic glutamate receptor (mGluR)-mediated long-term depression (LTD), we produced mouse lines in w

206 protein synthesis, enhanced mGluR-dependent long-term depression (LTD), weight gain, and macro-orchi

207 otropic glutamate receptor (mGluR)-dependent long-term depression (LTD), which has provided a general

208 ial for a form of synaptic plasticity termed long-term depression (LTD), which is implicated in neuro

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

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

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

212 gnetic brain stimulation technique to induce long-term depression (LTD)-like neuroplasticity.

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

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

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

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

217 (2+) have a crucial role in the induction of long-term depression (LTD).

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

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

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

221 asticity, such as long-term potentiation and long-term depression (LTD).

222 pression of long-term potentiation (LTP) and long-term depression (LTD).

223 est that synapses on such cells will undergo long-term depression (LTD).

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

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

226 interneurons exhibit robust activity-induced 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 he hippocampus, with abnormal enhancement of long-term depression mediated by metabotropic glutamate

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

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

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

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

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

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

239 I metabotropic glutamate receptors leads to long-term depression (mGluR-LTD).

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

241 in the induction of NMDA-receptor dependent long-term depression (NMDAR-LTD) in the hippocampus.

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

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

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

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

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

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

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

249 onstrated a novel activity-dependent form of long-term depression of electrical synapses in the TRN.

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

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

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

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

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

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

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

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

258 slices, activation of CB1 receptors induces long-term depression of inhibitory responses (iLTD) and

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

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

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

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

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

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

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

266 of GluK2-containing KARs that occurs during long-term depression of KAR-mediated synaptic transmissi

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

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

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

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

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

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

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

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

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

276 Instead of long-term depression, pep-19/pcp4-null mice exhibited lo

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

278 ha is required for endocannabinoid-dependent long-term depression (referred to as "i-LTD").

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

280 and postsynaptic hyperpolarization, whereas long-term depression relied on NMDA receptors and postsy

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

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

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

284 We observed long-term depression resulting from coordinated burst fi

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

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

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

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

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

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

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

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

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

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

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

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

297 1 activity is necessary for the induction of long-term depression, whereas downregulation of PP1 acti

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

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

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