ライフサイエンスコーパス: LTD

1 LTD induction requires CB1R in astroglial cells (but not

2 LTD of ovBNST neurons was prevented by a BDNF scavenger

3 LTD thus provides a cellular mechanism for information s

4 LTD was absent in CB1 knock-out mice but preserved in he

5 LTD, followed by precipitation and IDMS, allows for effi

6 LTD-like cortical plasticity is similar between AD and H

7 we observed a profound impairment in mGlu(3)-LTD following a single, 20-min restraint stress exposure

8 Our data suggest mGlu(3)-LTD is mediated by postsynaptic AMPAR internalization in

9 es (cysLTs), leukotriene (LT) C(4) (LTC(4)), LTD(4), and LTE(4), have different biologic half-lives,

10 nhanced glutamatergic activity and abolished LTD at vHipp to D1-MSN synapses.

11 Although ZIP has no effect on accumbal LTD in slices from naive or yoked saline mice, it is abl

12 the catalytically-dead mutant did not affect LTD induction.

13 KII can indeed mediate not only LTP but also LTD through regulated substrate selection; however, in t

14 During acute withdrawal, AIE altered LTD induced by the group I mGluR antagonist DHPG in fema

15 monstrate a direct role for amygdalocortical LTD in taste aversion learning.

16 CysLT(2)R binds LTC(4) and LTD(4)in vitro with similar affinities, but it displays

17 frequency AP-EPSP pairing, with both LTP and LTD absent under control conditions but present after SK

18 Additionally, LTP and LTD are correlated with dendritic spine enlargement and

19 We also demonstrate that, although LTP and LTD are normal in P21 arg(-/-) slices, both forms of pla

20 eakened output of D2-MSNs, occluding LTP and LTD at these synapses, respectively.

21 t-LTD were significantly larger than LTP and LTD obtained by modulating the frequency and duration of

22 Because the balance of LTP and LTD plays a critical role in activity-dependent synaptic

23 e synaptic modification threshold of LTP and LTD readjusts with activity and thus the outcome of syna

24 positive associative interaction of LTP and LTD, cross-capture, was altered in these mice.

25 ent to drive NMDA receptor-dependent LTP and LTD, respectively.

26 of the networks responsible for both LTP and LTD.

27 which both long-term potentiation (LTP) and LTD are possible.

28 signaling to drive both spine shrinkage and LTD.

29 of ion flow, in driving spine shrinkage and LTD.

30 on (6 month) basal synaptic transmission and LTD were also affected.

31 activation caused spine shrinkage as well as LTD in both genotypes.

32 We also assess the relationship between LTD and synaptic pruning in the context of recent findin

33 MCTRs blocked LTD(4)-initiated airway contraction in human precision-c

34 CA1 LTD as inhibition of JAK or STAT blocked LTD induction and prevented NMDA-induced AMPA (alpha-ami

35 ective CysLT(2)R antagonist and inhibited by LTD(4).

36 JAK-STAT signaling was critical for TA-CA1 LTD as inhibition of JAK or STAT blocked LTD induction a

37 TA-CA1 LTD requires NMDA receptor activation and is independent

38 rprised to find that mGluR activation causes LTD and AMPA receptor internalization, but no spine shri

39 Cerebellar LTD depends on the activation of calcium/calmodulin-depe

40 Mice with enhanced cerebellar LTD, due to double knockout (DKO) of MHCI H2-K(b)/H2-D(b

41 By contrast, LTD-induced spine removal of AKAP79/150 required its dep

42 DCS-LTD is abolished with an mGluR5 negative allosteric modu

43 in vitro induces a long-term depression (DCS-LTD) of excitatory synaptic strength in both human and m

44 from brief DCS application into durable DCS-LTD.

45 like reduction of cortical excitability (DCS-LTD), which has been tested in the treatment of epilepsy

46 However, DCS-LTD persists despite either gamma-aminobutyric acid type

47 cDCS reliably induced DCS-LTD in superficial cortical layers, and a long-term pote

48 ine/D-AP5 either produced a more uniform DCS-LTD throughout the cortical thickness or at least abolis

49 We tested, in vivo and in vitro, whether DCS-LTD occurs throughout the cortical thickness, and if not

50 dpoints were liver transplantation or death (LTD) and hepatopancreatobiliary malignancy, respectively

51 adult mouse hippocampus results in deficient LTD at CA3-CA1 synapses over a range of stimulation freq

52 -induced LTD but also blocked M(1)-dependent LTD in the PFC.

53 cal JAK-STAT signaling in activity-dependent LTD at TA-CA1 synapses and provide valuable insight into

54 A novel CB1-dependent LTD was induced in GABA cells that was dependent on meta

55 slices rescues the enhanced mGluR-dependent LTD phenotype observed in FXS mice.

56 ore both NMDA-dependent and mGluR5-dependent LTD in animals after cocaine self-administration and wit

57 and restore, neural trophism, NMDA-dependent LTD, and ultimately optimal learning.SIGNIFICANCE STATEM

58 ynaptic incorporation during NMDAR-dependent LTD.

59 Long-term potentiation (LTP) and depression (LTD) at glutamatergic synapses are intensively investiga

60 long-term potentiation (LTP) and depression (LTD) by affecting cellular and network excitability.

61 long-term potentiation (LTP) and depression (LTD) of excitatory synapse strength require the Ca(2+)/c

62 long-term potentiation (LTP) and depression (LTD), allows neurons to encode and respond to specific s

63 HIPP cells induces long-lasting-depression (LTD) of synaptic transmission but long-term-potentiation

64 Long-Term Potentiation (LTP) or Depression (LTD) respectively.

65 uR5-dependent long-term synaptic depression (LTD) in area CA1 of the hippocampus, but an effect on sp

66 Presynaptic long-term synaptic depression (LTD) plasticity at glutamatergic inputs to dorsal striat

67 lu1/5-induced long-term synaptic depression (LTD).

68 potentiation (LTP) and long-term depression (LTD) and homeostatic scaling.

69 ired induction of both long-term depression (LTD) and long-term potentiation (LTP).

70 lates the induction of long-term depression (LTD) and potentiation (LTP) at the PF-PC synapse.

71 MD selectively induces long-term depression (LTD) and shifts spike timing-dependent plasticity (STDP)

72 rm potentiation (LTP), long-term depression (LTD) and spike-timing dependent plasticity (STDP) are de

73 responses, pointing to long-term depression (LTD) as a mechanism for learning.

74 We show that long-term depression (LTD) at corticostriatal synapses of the direct pathway i

75 in activity-dependent long-term depression (LTD) at hippocampal Schaffer collateral (SC)-CA1 synapse

76 ial role for ASIC1a in long-term depression (LTD) at mouse insular synapses.

77 rkB signaling mediated long-term depression (LTD) at postsynaptic sites in ovBNST neurons.

78 In long-term depression (LTD) at synapses in the adult brain, synaptic strength i

79 Long-term depression (LTD) at these synapses is driven by climbing fibres (CFs

80 Long-term depression (LTD) between cortical layer 4 spiny stellate cells and l

81 potentiation (LTP) and long-term depression (LTD) can be induced at the same synaptic activation freq

82 tes, while optogenetic long-term depression (LTD) diminishes, the behavioral effect of aggression tra

83 naptic plasticity, the long-term depression (LTD) elicited by activation of type-I metabotropic gluta

84 an restore the loss of long-term depression (LTD) formation, counteract the reduction in NMDAR-mediat

85 potentiation (LTP) and long-term depression (LTD) forms that relay on the activation of NMDA receptor

86 The expression of long-term depression (LTD) in cerebellar Purkinje cells results from the inter

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

88 MDA receptor-dependent long-term depression (LTD) in the hippocampus.

89 tion of M(1)-dependent long-term depression (LTD) in the prefrontal cortex (PFC).

90 ggesting an inhibitory long-term depression (LTD) induced by an exogenous mu-opioid.

91 istribution of Inp54p, long-term depression (LTD) induced by low-frequency stimulation was blocked in

92 lastic facilitation of long-term depression (LTD) induction at hippocampal CA1 synapses.

93 reased mGluR5-mediated long-term depression (LTD) leading to several clinical trials of mGluR5 inhibi

94 potentiation (LTP) and long-term depression (LTD) mechanisms that rely on the activation of NMDA rece

95 ortical inputs induced long-term depression (LTD) mediated by adenosine A1 receptor (A1R) activation

96 munication by inducing long-term depression (LTD) of excitatory transmission at hippocampal CA3-CA1 s

97 ion of mGlu(3) induces long-term depression (LTD) of excitatory transmission in the PFC at inputs fro

98 ation of mGlu3 induces long-term depression (LTD) of excitatory transmission in the PFC at inputs fro

99 receptor D4-dependent long-term depression (LTD) of glutamatergic excitatory synapses by increasing

100 s) in conjunction with long-term depression (LTD) of synaptic strength.

101 potentiation (LTP) and long-term depression (LTD) to assess deficits in bidirectional synaptic plasti

102 vivo circuit-specific long-term depression (LTD) unmasks the therapeutic power of EE to achieve long

103 group I mGluR-mediated long-term depression (LTD) was disrupted at these timepoints.

104 This long-term depression (LTD) was mediated by the endocannabinoid 2-arachidonoyl

105 axed-out synapses, but long-term depression (LTD) was readily induced by low-frequency stimulation.

106 tentiation (LTP) or of long-term depression (LTD) were assessed using respectively intermittent (iTBS

107 (LTP)) or depression (long-term depression (LTD)) as well as the phosphorylation state of Ser831 and

108 potentiation (LTP) and long-term depression (LTD), and for the regulation of the majority of genes in

109 unctions now extend to long-term depression (LTD), and last year saw the first direct evidence for me

110 potentiation (LTP) or long-term depression (LTD), respectively.

111 glutamatergic synaptic long-term depression (LTD), without significant effects on chronic corticoster

112 ulation (cDCS) induces long-term depression (LTD)-like reduction of cortical excitability (DCS-LTD),

113 nduced NMDAR-dependent long-term depression (LTD).

114 c induction of in vivo long-term depression (LTD).

115 play impaired cortical long-term depression (LTD).

116 LTP) or removed during long-term depression (LTD).

117 obust activity-induced long-term depression (LTD).

118 Interestingly, late long-term depression (LTD; L-LTD) was not compromised, but the positive associ

119 The limited trypsin digestion (LTD) method has been developed and does not require stra

120 eals how PTPMEG cooperates with PKC to drive LTD expression by facilitating the effect of PKC on the

121 met during design of ligand-targeted drugs (LTDs) to achieve the required therapeutic potency with m

122 hippocampal synapses by anchored PKA during LTD induction but are then rapidly removed by anchored c

123 iently augment NMDAR Ca(2+) signaling during LTD induction.

124 ansient anchoring in dendritic spines during LTD induction.

125 ine how spines change their structure during LTD induced by activation of mGluRs or NMDA receptors (N

126 In contrast, eCB-LTD in PE animals was not rescued by increasing presynap

127 nnabinoid-mediated long-term depression (eCB-LTD) in VTA DA neurons.

128 Together, PE leads to impaired eCB-LTD at the excitatory synapses of VTA DA neurons primari

129 Mechanistic studies for impaired eCB-LTD revealed that PE downregulated CB1 receptor function

130 stently alters eCB signaling and impairs eCB-LTD at the excitatory synapses, an important synaptic pl

131 educed low-frequency stimulation-induced eCB-LTD.

132 Interestingly, eCB-LTD in PE animals was rescued by metabotropic glutamate

133 ortunities for innovating safe and effective LTDs has never been greater.

134 y preventing the adverse effect of excessive LTD on memory consolidation.

135 mediate frequencies, neurogranin facilitates LTD, but limits LTP by precluding binding of CaMKII with

136 and this astrocyte response is necessary for LTD.

137 3-driven gene transcription was required for LTD as inhibition of STAT3-DNA binding, nuclear export,

138 tic, not presynaptic NMDARs are required for LTD induction.

139 GSK3alpha, but not GSK3beta, is required for LTD.

140 ibition is both necessary and sufficient for LTD induction.

141 for relatively larger calcium transients for LTD than for LTP induction at any given stimulus frequen

142 r synaptic efficacy, which precluded further LTD induction.

143 rained to self-administer cocaine, GABAergic LTD was abolished in D2-, but not in D1-MSN synapses.

144 on at hippocampal CA3-CA1 synapses (O-GlcNAc LTD).

145 ng AMPARs, similar to expression of O-GlcNAc LTD.

146 el form of LTD at CA3-CA1 synapses, O-GlcNAc LTD.

147 It is noteworthy that glutamatergic LTD, which is known to exist on stratum lucidum interneu

148 n young animals and to uncover a hippocampal LTD-to-LTP shift.

149 lts identified lung MCTRs that blocked human LTD(4)-induced airway contraction and promoted resolutio

150 restingly, VU0453595 fully restored impaired LTD as well as deficits in cognitive function and social

151 The impaired LTD and extinction learning in ASIC1a null mice were res

152 f ZIP to reverse cocaine-induced deficits in LTD.

153 tic transmission or LTP, but participates in LTD.

154 rm-selective drugs to dissect their roles in LTD.

155 ional control, protein synthesis-independent LTD, neocortical hyperexcitability, audiogenic seizures,

156 oderate physiological stimulation can induce LTD.

157 irs of complex spikes are required to induce LTD.

158 ed to potentiate orthosteric agonist-induced LTD but also blocked M(1)-dependent LTD in the PFC.

159 unmasked persistent changes in DHPG-induced LTD and behavior that were not present under basal condi

160 of GSK3alpha and mediates GSK3alpha-induced LTD.

161 ation of DCN parallel fiber synapses induced LTD of synaptic zinc signaling (Z-LTD), evidenced by red

162 extinction of a cocaine-cue memory, induces LTD-like changes at T-LA synapses, and a corresponding d

163 abotropic glutamate (mGlu) receptors induces LTD of synaptic transmission at Schaffer collateral-CA1

164 e activation of the M1 mAChR subtype induces LTD in PFC and that this response is completely lost aft

165 Inhaled LTD(4) blocked LTC(4)-mediated potentiation of ovalbumin

166 restingly, late long-term depression (LTD; L-LTD) was not compromised, but the positive associative i

167 60, in the absence of APV, no or very little LTD was found in KO that was completely restored by appl

168 nstrate that the apparent differences in LTP/LTD magnitude seen across ages in AD transgenic mouse mo

169 adulthood, autophagy is up-regulated to make LTD induction harder, thereby preventing the adverse eff

170 iated response is necessary for A1R-mediated LTD.

171 e integral elements of striatal A1R-mediated LTD.SIGNIFICANCE STATEMENT Abnormal striatal circuit fun

172 We found that endocannabinoid/mGlu5-mediated LTD and NMDAR-dependent LTP were lacking in adult n-3-de

173 scovered that endocannabinoid/mGlu5-mediated LTD in the mPFC and accumbens was abolished in adult n-3

174 MDARs and their regulation of mGluR-mediated LTD at different developmental stages using several diff

175 a phenomenon exhibited during mGluR-mediated LTD.

176 ogy of FXS leading to altered mGluR-mediated LTD.

177 that express alcohol-sensitive MOR-mediated LTD (mOP-LTD) in DLS.

178 d we observed a profound impairment in mGlu3-LTD following a single, 20-min restraint stress exposure

179 Our data suggest mGlu3-LTD is mediated by postsynaptic AMPAR internalization in

180 mGluR-LTD reduces synaptic strength and is relevant to learnin

181 mGluR-LTD was associated with calpain-1 activation following T

182 ion of GluN2B, but not GluN2A, blocked mGluR-LTD only in WT.

183 Consistently, mGluR-LTD was impaired in calpain-1 KO mice, and the impairmen

184 mGluR long-term depression (mGluR-LTD) is a form of synaptic plasticity induced at excitat

185 mGluR-dependent long-term depression (mGluR-LTD), a key biomarker in the disease, at four different

186 eceptor-mediated long-term depression (mGluR-LTD)-whose disruption is postulated to increase vulnerab

187 d late phase of Arc translation during mGluR-LTD, through a mechanism involving mTOR and ribosomal pr

188 t the underlying cause of the enhanced mGluR-LTD in KO (at p30) is caused by dysregulated NMDAR signa

189 cessive protein synthesis, exaggerated mGluR-LTD, and audiogenic seizures.

190 otypical RNA granule substrate and for mGluR-LTD in hippocampal neurons.

191 hat calpain-1 plays a critical role in mGluR-LTD and is involved in many forms of synaptic plasticity

192 merging as important control points in mGluR-LTD, a form of synaptic plasticity that is compromised i

193 , including NMDA receptors (NMDAR), in mGluR-LTD.

194 Interestingly, AKT activity inhibits mGluR-LTD, with overlapping functions for AKT1 and AKT3.

195 activation of Type I mGluRs and, like mGluR-LTD but unlike NMDAR-dependent plasticity, depends cruci

196 ocalization protein STAU2 in mediating mGluR-LTD through the regulation of mRNA translation complexes

197 of LTD that depends on Type I mGluRs (mGluR-LTD), but not NMDARs, has been implicated in learning de

198 pe-I metabotropic glutamate receptors (mGluR-LTD).

199 n the KO where blocking GluN2B rescued mGluR-LTD, suggesting GluN2B-containing NMDARs in the KO are h

200 At all other age groups tested, mGluR-LTD was almost identical between KO and WT.

201 We found that contrary to DLS, DMS mOP-LTD is induced by activation of MORs at inputs from both

202 Here, we explore mOP-LTD in DMS using mouse brain slice electrophysiology.

203 ress alcohol-sensitive MOR-mediated LTD (mOP-LTD) in DLS.

204 Furthermore, only mOP-LTD at cortical inputs was sensitive to alcohol's delete

205 ected, in the presence of APV, we found more LTD in the mouse KO than in WT.

206 Because most LTDs are composed of a targeting ligand (e.g., organic m

207 Consistent with altered NAc LTD, TLR4.KO animals exhibit an attenuation in drug rewa

208 this association because pHFD abolishes NMDA-LTD, a function that is restored by RELN overexpression.

209 partate-dependent long-term depression (NMDA-LTD) at prefrontal excitatory synapses as a synaptic sig

210 ceptor-dependent long-term depression (NMDAR-LTD) is a long-lasting form of synaptic plasticity.

211 Autophagy is inhibited during NMDAR-LTD to decrease endocytic recycling.

212 In NMDAR-LTD, however, they are diverted to late endosomes for de

213 Additionally, the inducibility of NMDAR-LTD is greatly reduced in adulthood.

214 duction and developmental dampening of NMDAR-LTD.

215 LTC(4), but not LTD(4), strongly potentiates allergen-induced pulmonary

216 ns of Delta(9)-tetrahydrocannabinol occluded LTD compared with vehicle injections; however, a single

217 The administration of LTD(4) to Ptges(-/-) mice, which display enhanced LTC(4)

218 riatum-dependent behaviors and disruption of LTD influences action control.

219 mote the expression of LTP at the expense of LTD, and Gq-coupled receptors promote LTD at the expense

220 ion, long-term potentiation or expression of LTD.

221 tress can elicit metaplastic facilitation of LTD induction as authentic stress.SIGNIFICANCE STATEMENT

222 pruning in the context of recent findings of LTD dysregulation in several mouse models of autism spec

223 sing O-GlcNAcylation induces a novel form of LTD at CA3-CA1 synapses, O-GlcNAc LTD.

224 However, only the mGluR-dependent form of LTD has been characterized.

225 In young rodents, this form of LTD has been repeatedly reported to require presynaptic

226 Indeed, dysfunction of a form of LTD that depends on Type I mGluRs (mGluR-LTD), but not N

227 und that ZIP was able to rescue two forms of LTD in cocaine-experienced mice.

228 and STAT3 accompanied chemical induction of LTD and AMPA receptor internalization.

229 selective potentiation of M1 on induction of LTD and behavioral deficits in PCP-treated mice.

230 ciation of a novel tastant with induction of LTD at the BLA-GC input in vivo was sufficient to change

231 PIP2 is critically required for induction of LTD whereas translocation of Inp54p to plasma membranes

232 equencies, neurogranin inhibits the onset of LTD by limiting CaN activation.

233 ASIC1a reduced the induction probability of LTD without affecting that of long-term potentiation in

234 olitis) were associated with a lower risk of LTD (unadjusted hazard ratio [HR], 0.62; P < .001 and HR

235 sex was also associated with a lower risk of LTD or malignancy (HR, 0.88; P = .002 and HR, 0.68; P <

236 duct PSC was associated with a lower risk of LTD or malignancy compared with classic PSC (HR, 0.30 an

237 However, optogenetic LTD applied to this projection in vivo transiently re-si

238 Instructive signals determine whether LTP or LTD is induced, by modulating local calcium transients.

239 vanished >50 Hz or <1 Hz (where only LTP or LTD occurred).

240 vidual synapses expressed significant LTP or LTD, but the average over all synapses did not change.

241 ke cortical plasticity forming a paradoxical LTD in comparison to HS.

242 ur model advances the understanding of PF-PC LTD regulation and induction, and provides a validated e

243 F stimulus onset were required to trigger PF-LTD, which is consistent with the requirements for eyebl

244 somatodendritic profiles throughout the PPT/LTD complex.

245 export, and gene transcription all prevented LTD induction.

246 both frequencies, buffering calcium prevents LTD induction and LTP results instead, identifying the e

247 ynaptic, but not presynaptic NMDARs prevents LTD induction.

248 ion of GluN2B receptors would compromise pRh LTD, leading to loss of NOR memory.

249 ation resulted in an inability to induce pRh LTD following 1 Hz stimulation, an effect that was rever

250 Ro 25-6981 prevented DCS restoration of pRh LTD in meth subjects.

251 nse of LTD, and Gq-coupled receptors promote LTD at the expense of LTP.

252 her enhances calcium transients and promotes LTD.

253 scribed AKAP79/150 trafficking in regulating LTD-induced spine shrinkage.

254 Optogenetic stimulation designed to saturate LTD produced the same impairment in WT as observed in DK

255 Both st-LTP and st-LTD required NMDA receptors, but st-LTP also required re

256 Importantly, st-LTP and st-LTD were significantly larger than LTP and LTD obtained

257 m potentiation and depression (st-LTP and st-LTD) were confined to a +/-25 ms time-window.

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

259 ession results in impaired mGluR5-stimulated LTD.

260 s and an augmented low-frequency stimulation LTD of the pathway, suggesting that there is a functiona

261 Notably, such LTD-induced depalmitoylation was also blocked by CaMKII

262 However, the induction of synaptic LTD is suppressed in Pyk2-null slices.

263 ike-timing-dependent long-term depression (t-LTD) in vivo.

264 During t-LTD a single astrocyte acts as a delay factor for fast n

265 oupled with calcineurin signaling, induces t-LTD which is sensitive to the temporal difference betwee

266 and astrocytic sites to the time window of t-LTD induction.

267 e-mediated molecular mechanisms underlying t-LTD and link complex biochemical networks at presynaptic

268 ulopontine (PPT) and laterodorsal tegmental (LTD) nuclei of the mesopontine tegmentum (MPT).

269 Here we demonstrate that LTD at adult TA-CA1 synapses involves JAK-STAT signaling

270 We show that LTD at inhibitory synapses is dependent on downstream cA

271 Model simulations show that LTD expression is increased by serine/threonine phosphat

272 Here we review evidence suggesting that LTD and synaptic pruning share components of their under

273 The LTD by single pyramidal cell 40 Hz spike bursts is speci

274 The LTD of VLE connections alters suprathreshold activation

275 ether LTD or LTP is evoked but, instead, the LTD threshold slides, thus preserving the requirement fo

276 receptors was responsible for occluding the LTD.

277 te significantly to the decisive role of the LTD and PPT in sleep-wakefulness.

278 In this study, we tested the LTD-IDMS assay on A(H5N1) vaccine material that had been

279 The results showed that the LTD-IDMS method effectively quantified the potent HA in

280 Thus, LTD in HIPPs may assist flow of spatial information from

281 The conversion of LTC(4) to LTD(4) may limit the duration and extent of potentially

282 B inhibitors, indicating the contribution to LTD induction.

283 ke timing-dependent plasticity (STDP) toward LTD at GABAergic synapses onto VTA DA neurons through ep

284 er-Purkinje cell synapses, which can undergo LTD or LTP in response to 1-Hz and 100-Hz stimulation.

285 , while MF glutamatergic responses underwent LTD, the simultaneous MF GABAergic responses of stratum

286 Using LTD as a readout of persistent synaptic consequences of

287 inhibitory GABAergic synapses and an in vivo LTD of excitatory glutamatergic synapses.

288 at favors phosphorylation by prolonged, weak LTD stimuli versus brief, strong LTP stimuli.

289 h actually led to LTP in PE animals, whereas LTD was still observed in controls.

290 te calcium amplitudes that determine whether LTD or LTP is evoked but, instead, the LTD threshold sli

291 tion of AMPA receptors can determine whether LTD or LTP occurs in cerebellar PCs.

292 We sought to determine whether LTD(4) functionally antagonizes LTC(4) signaling at CysL

293 spectrum disorder (ASD) and discuss whether LTD deficits can indicate impaired pruning processes tha

294 ere that the spine shrinkage associated with LTD indeed requires synaptic AKAP79/150 removal, which i

295 itment, removal, or activity interferes with LTD.

296 ce to loud sound caused G1 mGluR-dependent Z-LTD at DCN parallel fiber synapses, thus validating our

297 ic Ca(2+) are necessary and sufficient for Z-LTD induction.

298 n is necessary and sufficient for inducing Z-LTD and Z-LTP.

299 es induced LTD of synaptic zinc signaling (Z-LTD), evidenced by reduced zinc-mediated inhibition of E

300 ensor probing zinc release, supported that Z-LTD is expressed, at least in part, via reductions in pr