ライフサイエンスコーパス: mGluR

1 mGluR activation also transiently increased the amplitud

2 mGluR activation produced long-term changes in the subth

3 mGluR long-term depression (mGluR-LTD) is a form of syna

4 mGluR-LTD in ArcGFP+ neurons required rapid protein synt

5 mGluR-LTD priming in neurons with similar Arc activation

6 mGluR-LTD reduces synaptic strength and is relevant to l

7 mGluR-LTD was associated with calpain-1 activation follo

8 raction we showed to be regulated by group 1 mGluR activation.

9 that cue-elicited deficits in vmPFC group 1 mGluR function mediate resistance to extinction during p

10 protein, alpha-actinin-4, as a novel group 1 mGluR-interacting partner that orchestrates spine dynami

11 alleled with increased expression of Group 1 mGluR-related genes Homer 1a and Arc.

12 Group 1 mGluRs (mGluR1a and mGluR5) are coupled primarily to Gal

13 longation and turnover stimulated by group 1 mGluRs despite intact surface receptor expression and do

14 other glutamated substrates, which activate mGluR I.

15 Activated mGluR I subsequently induces activation of phosphoinosit

16 Given that IMP is not thought to affect mGluRs, behavioral detection of l-glutamate appears to r

17 Recent reports indicate altered mGluR signaling in various tumor types, and several soma

18 he pathophysiology of FXS leading to altered mGluR-mediated LTD.

19 issecting the functional impact of amygdalar mGluR-plasticity on fear versus anxiety in health and di

20 ings from horizontal cells, we found that an mGluR agonist (L-AP4) reduced cone-driven light response

21 for drep-2 learning deficits, and drep-2 and mGluR learning phenotypes behaved non-additively, sugges

22 tial molecular link between inflammation and mGluR-mediated sensitization.

23 paired burst spiking in coupled neurons, and mGluR-dependent tetanization of synaptic input - are sep

24 ently uncovered cooperation between mERs and mGluRs is functional in males where it mediates the acut

25 ch signaling through both NMDA receptors and mGluRs is required to drive activity-dependent synaptic

26 receptors, together with internal stores and mGluRs, control the direction of plasticity at interneur

27 r antagonists, a TREK-1 receptor antagonist, mGluR antagonists and (2R,6R)-HNK.

28 enerate light-agonized and light-antagonized mGluRs (LimGluRs).

29 nhibition of GluN2B, but not GluN2A, blocked mGluR-LTD only in WT.

30 , we show that modifications induced by both mGluR groups converge on the same signaling cascade--ade

31 gic transmission, and the LTD was blocked by mGluR II antagonist, indicating that synaptic activation

32 cAMP levels can be regulated by mGluR signaling.

33 terosynaptic long-term plasticity induced by mGluRs at inhibitory synapses.

34 lso required reinforcing signals mediated by mGluRs and intracellular calcium stores.

35 rect phosphorylation of eIF2alpha, bypassing mGluR activation, triggered a sustained LTD and removal

36 Consistent with compromised mGluR-LTD, MK2/3 DKO mice have distinctive deficits in h

37 Consistently, mGluR-LTD was impaired in calpain-1 KO mice, and the imp

38 In contrast, mGluR-dependent plasticity is independent of calcium ent

39 lly displayed long-term synaptic depression (mGluR-LTD) and robust increases in dendritic Arc protein

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

41 ors on mGluR-dependent long-term depression (mGluR-LTD), a key biomarker in the disease, at four diff

42 mate receptor-mediated long-term depression (mGluR-LTD)-whose disruption is postulated to increase vu

43 Cdh1-APC operates in the cytoplasm to drive mGluR-LTD.

44 lated protein; a phenomenon exhibited during mGluR-mediated LTD.

45 rly and late phase of Arc translation during mGluR-LTD, through a mechanism involving mTOR and riboso

46 the mRNAs translationally upregulated during mGluR-LTD.

47 g that Drep 2 might be involved in effective mGluR signaling.

48 interactions with long-form Homers enhanced mGluR-induced epileptiform burst firing in wild-type (WT

49 The peptide enhanced mGluR-evoked endocannabinoid (eCB)-mediated suppression

50 t in hippocampal slices rescues the enhanced mGluR-dependent LTD phenotype observed in FXS mice.

51 ts that the underlying cause of the enhanced mGluR-LTD in KO (at p30) is caused by dysregulated NMDAR

52 The presence of an ER-mGluR interaction in birds suggests that this mechanism

53 -specific estrogen receptor alpha (ERalpha), mGluR, and endocannabinoid-dependent mechanism.

54 intracellular signaling that links ERalpha, mGluRs, and endocannabinoids in females and identify whe

55 In particular, exaggerated mGluR-dependent LTD is featured in fragile X syndrome, b

56 ing excessive protein synthesis, exaggerated mGluR-LTD, and audiogenic seizures.

57 Focal mGluR activation in L5, near the soma or at the border o

58 Following mGluR stimulation with (S)-3,5-dihydroxyphenylglycine, t

59 a prototypical RNA granule substrate and for mGluR-LTD in hippocampal neurons.

60 owever, no crossed blockade was detected for mGluR or mAchR effects on interneuron after-burst potent

61 = 50 without ASD), all haploinsufficient for mGluR network gene RANBP1, were evaluated for "second mG

62 Furthermore, mGluR-LTD is impaired in the hippocampus of MK2/3 double

63 ording system, we showed that activating Gp1 mGluR elevates neural network activity, as demonstrated

64 Dysregulated Gp1 mGluR signaling has been observed in numerous neurologic

65 double minute-2 (Mdm2), is required for Gp1 mGluR-induced translation and neural network activity.

66 wever, the molecular pathways underlying Gp1 mGluR-dependent plasticity mechanisms are complex and ha

67 ubiquitination and down-regulation upon Gp1 mGluR activation.

68 data revealed a novel mechanism by which Gp1 mGluR and FMRP mediate protein translation and neural ne

69 entified a novel mechanism through which Gp1 mGluR mediates protein translation and neural plasticity

70 ain circuit excitability associated with Gp1 mGluR in neurological diseases such as FXS.

71 te binge alcohol-induced increases in Group1 mGluR signaling within the CeA as a neuroadaptation main

72 11.5% of ASD had mGluR CNV's vs. 3.2% in controls (p < 0.001).

73 neral approach to characterize heterodimeric mGluRs, our study opens new avenues to understanding the

74 lusive homodimers, 16 possible heterodimeric mGluRs have been proposed but their existence in native

75 Augmented hippocampal mGluR-induced long-term depression (LTD; or chemically i

76 , a behavioral task that induces hippocampal mGluR-LTD in vivo.

77 While pressure ejection of the group I mGluR (mGluR1/5) agonist DHPG [(S)-3,5-dihydroxyphenylgl

78 nregulation of FMRP was dependent on group I mGluR activation and was blocked by a proteasome inhibit

79 We compared the action of group I mGluR activation on several populations of striatal neur

80 ne populations demonstrated that the group I mGluR agonist (RS)-3,5-dihydroxyphenylglycine (DHPG) rob

81 n MSNs of "incubated rats" using the group I mGluR agonist (S)-3,5-dihydroxyphenylglycine in combinat

82 s in females than males, whereas the group I mGluR agonist DHPG increases IP3 levels equivalently in

83 rgic axons, or by application of the group I mGluR agonist dihydroxyphenylglycine, paired with postsy

84 s and evoked responses, we show that group I mGluR agonists act presynaptically to increase neurotran

85 P also depends on activation of both group I mGluR and M1 mAChRs.

86 leptiform discharges were blocked by group I mGluR antagonists (LY367385 + MPEP) and their induction

87 These findings support the use of group I mGluR antagonists as a potential therapy that extends to

88 and this deficit was not rescued by group I mGluR antagonists.

89 inal tail of mGluR1 (a member of the group I mGluR family) plays crucial role in this process.

90 findings extend our understanding on group I mGluR influence of striatal output via powerful, local G

91 The group I mGluR selective agonist (S)-3,5-dihydroxyphenylglycine (

92 the molecular mechanisms underlying Group I mGluR signaling is important for understanding physiolog

93 l (Fmr1(-/-)) of fragile X syndrome, group I mGluR-activated translation is exaggerated causing enhan

94 lding protein spinophilin as a novel Group I mGluR-interacting protein.

95 ation facilitated the recruitment of group I mGluR-mediated prolonged epileptiform discharges.

96 syndrome, it remains unknown whether group I mGluR-mediated protein synthesis is involved in any beha

97 ion of FMRP led to enhanced synaptic group I mGluR-mediated translation.

98 zation of eCB biosynthetic enzyme and type I mGluR mRNA in VTA neurons.

99 ate released from the IHCs activates group I mGluRs (mGluR1s), probably present on the efferent termi

100 amined possible interactions between group I mGluRs and mAChRs in anti-Hebbian LTP at synapses which

101 C efferent inhibition is mediated by group I mGluRs and specifically by mGluR1s.

102 t role in regulating the activity of Group I mGluRs as well as their influence on synaptic activity.

103 triggered by exogenous activation of group I mGluRs at the same time as the interneuron is hyperpolar

104 that interaction of spinophilin with Group I mGluRs attenuates receptor endocytosis and phosphorylati

105 results suggest that stimulation of group I mGluRs during glutamate exposure caused proteolysis of F

106 Stimulation of group I mGluRs elicits several forms of translation-dependent ne

107 Here we show that activation of Group I mGluRs in medium spiny neurons induces trafficking of Gl

108 t ligand-mediated internalization of group I mGluRs is ubiquitination-dependent.

109 demonstrate for the first time that group I mGluRs mediate inflammation-induced sensitization to neu

110 We found that blockade of either group I mGluRs or M1 mAChRs prevented the induction of anti-Hebb

111 Here we test whether group I mGluRs require beta-arrestin signalling during specific

112 Activation of group I mGluRs rescues synaptic plasticity and restores small-co

113 veal a signalling pathway engaged by group I mGluRs to effect changes in synaptic and cell intrinsic

114 protein-coupled receptors, including group I mGluRs, are present in lipid rafts, but the mechanisms u

115 ubiquitination in the regulation of group I mGluRs, as well as its role in mGluR-dependent AMPAR end

116 -dependent activation of ERK-MAPK by group I mGluRs, suggesting a potential function for cholesterol

117 pe voltage-gated Ca(2+) channels, or group I mGluRs.

118 isms that control the trafficking of group I mGluRs.

119 ent inhibition via the activation of group I mGluRs.

120 erminal PDZ binding motif encoded by Group I mGluRs.

121 ail and second intracellular loop of Group I mGluRs.

122 tion of a form of LTD that depends on Type I mGluRs (mGluR-LTD), but not NMDARs, has been implicated

123 is form of LTP requires activation of Type I mGluRs and, like mGluR-LTD but unlike NMDAR-dependent pl

124 sented in children with syndromic ASD and if mGluR "second hit" confers additional risk for ASD in 22

125 DMV microinjections of the group II mGluR agonist APDC and whole cell recordings of excitato

126 of excitatory synaptic terminals to group II mGluR agonist.

127 rs to the brain BCI-632, the active Group II mGluR antagonist metabolite.

128 ronic pharmacological inhibition of Group II mGluR in Dutch APP (Alzheimer's amyloid precursor protei

129 Group II mGluR inhibition may offer a unique package of relevant

130 later by divergence of group I and group II mGluR versus group III in l-SOP responses.

131 Conversely, activation of the Group II mGluR, mGluR3, induces long-term potentiation of electri

132 I metabotropic glutamate receptors (Group II mGluR: mGlu2, mGlu3) are reported to stimulate neurogene

133 Local application of group I or I/II mGluR agonists or adenosine triphosphate (ATP) elicited

134 specially mGluR4,-6,-8 but not group I or II mGluR.

135 cological or synaptic activation of group II mGluRs (mGluR II) induces LTD at GABAergic synapses with

136 r examined whether these effects of group II mGluRs are through the regulation of NMDAR exocytosis vi

137 The activation of group II mGluRs caused a significant enhancement of NMDAR current

138 cond aim was to investigate whether group II mGluRs similarly influence the response of vagal motoneu

139 Inhibition of brainstem group II mGluRs, however, uncovers the ability of OXT to modulate

140 rlying the antipsychotic effects of group II mGluRs, we examined their impact on NMDA receptors (NMDA

141 mechanism of full-length mammalian group II mGluRs.

142 The net effect of group III mGluR activation at these synapses is to suppress thalam

143 lly via systemic administration of group III mGluR antagonists, successfully re-established theta coo

144 luR7 differs from mGluR4 and other group III mGluR in that L-glutamate and L-SOP activate it with low

145 t, mGluR4 has in common with other group III mGluR that it is activated with higher potency and effic

146 (L-SOP), which strongly activates group III mGluR, especially mGluR4,-6,-8 but not group I or II mGl

147 Blocking group II/III mGluRs eliminated the inhibitory effect of oxotremorine-

148 and generate seven light-gated group II/III mGluRs, including variants of mGluR2, 3, 6, 7, and 8.

149 through indirectly stimulating group II/III mGluRs.

150 ies, the Cdh1 knockout phenotype of impaired mGluR-LTD.

151 ndogenous FMRP, and knockout of Cdh1 impairs mGluR-induced ubiquitination and degradation of FMRP in

152 oting complex (Cdh1-APC), profoundly impairs mGluR-LTD in the hippocampus.

153 Importantly, mGluRs have been shown to be critical for acquisition of

154 enocopy Fmr1(-/y) mice in the alterations in mGluR-dependent long-term depression, basal protein synt

155 0% with 22q11.2DS + ASD had "second hits" in mGluR network genes vs 2% in 22q11.2DS-ASD (p < 0.014).

156 d basal protein synthesis and an increase in mGluR-dependent long-term depression in CA1 of the hippo

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

158 are emerging as important control points in mGluR-LTD, a form of synaptic plasticity that is comprom

159 ic patients shows a significant reduction in mGluR(2) transcripts compared to control subjects, sugge

160 was done via blinded medical chart review in mGluR positive and randomly selected mGluR negative case

161 on of group I mGluRs, as well as its role in mGluR-dependent AMPAR endocytosis.

162 cate that calpain-1 plays a critical role in mGluR-LTD and is involved in many forms of synaptic plas

163 -term depression (LTD; or chemically induced mGluR-LTD) in Eif4ebp2(-/-) mice was rescued by mGluR1 o

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

165 Age-unimpaired rats, in contrast, had intact mGluR LTD.

166 Crystal structures of isolated mGluR LBD dimers led to the suggestion that activation a

167 hat misregulation of Cyfip2 function and its mGluR-induced expression contribute to the neurobehavior

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

169 Mechanistically, mGluR activation induced mRNA translation-dependent incr

170 RNA localization protein STAU2 in mediating mGluR-LTD through the regulation of mRNA translation com

171 a form of LTD that depends on Type I mGluRs (mGluR-LTD), but not NMDARs, has been implicated in learn

172 l or synaptic activation of group II mGluRs (mGluR II) induces LTD at GABAergic synapses without affe

173 metabotropic receptor, LimGluR3, with a new mGluR-specific PTL, D-MAG0460.

174 ception of a rebound depolarization, and non-mGluR-mediated long-term potentiation is unaltered.

175 y of Homer scaffolds is essential for normal mGluR-eCB functioning and that aberrant eCB signaling re

176 nist, indicating that synaptic activation of mGluR II induced the LTD.

177 utants, shown to benefit from attenuation of mGluR signaling, profited from the elimination of drep-2

178 mice, resulting in selective augmentation of mGluR-dependent depression.

179 Using heterologous expression of mGluR cDNA in rat sympathetic neurons from the superior

180 monstrated by a dose-dependent inhibition of mGluR-1-mediated thermal hyperalgesia and by colocalizat

181 hese findings indicate that the integrity of mGluR-LTD at A/C --> CA3 inputs may play a crucial role

182 ce, in adulthood, also restores the level of mGluR-dependent LTD to that observed in wild-type animal

183 Our findings identify a new model of mGluR-LTD, which promises to be of value in the treatmen

184 Normalization of mGluR(2) function within this brain circuit may be of th

185 study examines cocaine-induced plasticity of mGluR-dependent currents in dopamine neurons in the subs

186 translation of Arc underlies the priming of mGluR-LTD.

187 e we focus on NMDARs and their regulation of mGluR-mediated LTD at different developmental stages usi

188 tein translation inhibitors on the switch of mGluR function in MSNs of "incubated rats" using the gro

189 promises to be of value in the treatment of mGluR-LTD-linked cognitive disorders.

190 rt a general mechanism for the activation of mGluRs in which agonist binding induces closure of the L

191 utamate release sites to allow activation of mGluRs on the efferent terminals by glutamate spillover.

192 lead to a model of cooperative activation of mGluRs that provides a framework for understanding how c

193 and the other one based on the activation of mGluRs.

194 and the other one based on the activation of mGluRs.

195 +) channels, also requires the activation of mGluRs.

196 Pharmacological manipulation of mGluRs with effector-biased ligands could lead to novel

197 es of systemically injected PAMs and NAMs of mGluRs in rodents and monkeys, focusing on whether they

198 We conclude that PAMs and NAMs of mGluRs should be considered for clinical trials.

199 ts from rat studies in which PAMs or NAMs of mGluRs were injected intracranially to reduce drug self-

200 PAMs and NAMs of mGluRs, either of which can inhibit evoked glutamate rel

201 and negative allosteric modulators (NAMs) of mGluRs.

202 Chronic pharmacological stimulation of mGluRs compensated for drep-2 learning deficits, and dre

203 Trafficking of mGluRs plays an important role in controlling the precis

204 e investigated the role of NMDA receptors on mGluR-dependent long-term depression (mGluR-LTD), a key

205 me and Tuberous Sclerosis, the role of other mGluRs and their associated signaling network genes in s

206 lled by eIF2alpha phosphorylation, prevented mGluR-LTD and the internalization of surface AMPA recept

207 Metabotropic glutamate receptor (mGluR) 5 signaling activates ERK1/2.

208 e striatum, metabotropic glutamate receptor (mGluR) activation leads to several modulatory effects in

209 to group 1 metabotropic glutamate receptor (mGluR) activation, ArcGFP+ neurons preferentially displa

210 by group I metabotropic glutamate receptor (mGluR) activation.

211 roup II/III metabotropic glutamate receptor (mGluR) antagonists in wild-type mice.

212 atment with metabotropic glutamate receptor (mGluR) antagonists or lithium.

213 group I/II metabotropic glutamate receptor (mGluR) antagonists reduced the amplitude of the Ca(2+) t

214 The metabotropic glutamate receptor (mGluR) is required in ISCs for this response, and for an

215 lar GPCR, a metabotropic glutamate receptor (mGluR), can reduce cone synaptic transmission via Gbetag

216 nt with the metabotropic glutamate receptor (mGluR)-5 antagonist MTEP.

217 nthesis and metabotropic glutamate receptor (mGluR)-dependent long-term depression that, unlike in th

218 asal state, metabotropic glutamate receptor (mGluR)-induced dendritic spine regulation was impaired i

219 in group I metabotropic glutamate receptor (mGluR)-mediated suppression of synaptic transmission fro

220 lly via the metabotropic glutamate receptor (mGluR).

221 of Group 1 metabotropic glutamate receptor (mGluR).

222 ntrast, the metabotropic glutamate receptor (mGluR)5 antagonist MPEP [2-methyl-6-(phenylethynyl)pyrid

223 Group II metabotropic glutamate receptors (mGluR) decrease synaptic transmission to pancreas-projec

224 icities of metabotropic glutamate receptors (mGluR), we have examined the ability of representative m

225 of type-I metabotropic glutamate receptors (mGluR-LTD).

226 The metabotropic glutamate (Glu) receptors (mGluRs) play key roles in modulating excitatory neurotra

227 of Group I metabotropic glutamate receptors (mGluRs) activates signaling cascades, resulting in calci

228 ic group I metabotropic glutamate receptors (mGluRs) and Ca(2+) -permeable AMPA receptors.

229 ivation of metabotropic glutamate receptors (mGluRs) and muscarinic acetylcholine receptors.

230 group III metabotropic glutamate receptors (mGluRs) and, thus, is of interest as a potential biomark

231 principle, metabotropic glutamate receptors (mGluRs) are also suitable to convert synaptic activity i

232 gh group 1 metabotropic glutamate receptors (mGluRs) are critical for spine remodeling under physiopa

233 Metabotropic glutamate receptors (mGluRs) are dimeric class C GPCRs that modulate neuronal

234 Metabotropic glutamate receptors (mGluRs) are mainly known for regulating excitability of

235 Metabotropic glutamate receptors (mGluRs) are mandatory dimers playing important roles in

236 Metabotropic glutamate receptors (mGluRs) are, in principle, also suitable to trigger bidi

237 ivation of metabotropic glutamate receptors (mGluRs) by general and group I-specific mGluR agonists e

238 group I/II metabotropic glutamate receptors (mGluRs) during suprathreshold TBS resulted in a slight r

239 Metabotropic glutamate receptors (mGluRs) function as dimers.

240 of group I metabotropic glutamate receptors (mGluRs) induces long-term depression (LTD), which requir

241 of Group I metabotropic glutamate receptors (mGluRs) induces long-term depression of electrical synap

242 of group I metabotropic glutamate receptors (mGluRs) mGluR1 and mGluR5 reverses the autistic phenotyp

243 ceptors or metabotropic glutamate receptors (mGluRs) or orthosteric agonists of mGluR2/3.

244 Group I metabotropic glutamate receptors (mGluRs) play important roles in various neuronal process

245 f synaptic metabotropic glutamate receptors (mGluRs) reactivates translation of these particular mRNA

246 resynaptic metabotropic glutamate receptors (mGluRs) regulate cone photoreceptor synaptic transmissio

247 his to the metabotropic glutamate receptors (mGluRs) to generate light-agonized and light-antagonized

248 up 1 (Gp1) metabotropic glutamate receptors (mGluRs), including mGluR1 and mGluR5, elicits translatio

249 the eight metabotropic glutamate receptors (mGluRs), mGluR5 is the most highly expressed in neural s

250 ties among metabotropic glutamate receptors (mGluRs), we combined computational approaches with mutag

251 on class C metabotropic glutamate receptors (mGluRs), we map dimerization determinants and define a h

252 of group I metabotropic glutamate receptors (mGluRs), which have been previously used in other ASD mo

253 including metabotropic glutamate receptors (mGluRs), which in turn interact with the scaffolding pro

254 ic group I metabotropic glutamate receptors (mGluRs), which in turn rapidly facilitates local NMDA re

255 ight-gated metabotropic glutamate receptors (mGluRs).

256 as type I metabotropic glutamate receptors (mGluRs).

257 lized with metabotropic glutamate receptors (mGluRs).

258 he group 1 metabotropic glutamate receptors (mGluRs).

259 bility via metabotropic glutamate receptors (mGluRs).

260 ynapses by metabotropic glutamate receptors (mGluRs).

261 ly ablated metabotropic glutamate receptors (mGluRs, especially mGluR5) in developing cortical astrog

262 ctivation of group I metabotropic receptors (mGluRs) is required for anti-Hebbian LTP induction in in

263 played by group III metabotropic receptors (mGluRs), which are uniquely located in the presynaptic a

264 Pdyn expression during normal aging reduces mGluR expression and signaling, which in turn impairs co

265 X syndrome, but the mechanisms that regulate mGluR-LTD remain incompletely understood.

266 l ubiquitin signaling pathway that regulates mGluR-LTD in the brain.

267 agonist activity at mGlu2 over the remaining mGluR subtypes.

268 Remarkably, mGluR-dependent increase of PSD95 synthesis is abolished

269 have examined the ability of representative mGluR of group I, II, and III to be activated by endogen

270 rast in the KO where blocking GluN2B rescued mGluR-LTD, suggesting GluN2B-containing NMDARs in the KO

271 ol seeking, which was abolished by restoring mGluR(2) expression in the infralimbic cortex via viral-

272 work gene RANBP1, were evaluated for "second mGluR hits".

273 view in mGluR positive and randomly selected mGluR negative cases.

274 r mGluR5) and 10 mum LY341495 (non-selective mGluR blocker), but not by 80 mum AP5 (NMDA receptor blo

275 ors (mGluRs) by general and group I-specific mGluR agonists enhances IHC efferent inhibition.

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

277 ompared to control subjects, suggesting that mGluR(2) loss in the rodent and human corticoaccumbal ne

278 We show that mGluRs regulate light response encoding across the cone

279 First, we applied the mGluR agonist 3,5-dihydroxyphenylglycine in the absence

280 At a low concentration, the mGluR agonist did not generate eCBs at excitatory synaps

281 ore, acute knockdown of Siah-1A enhances the mGluR-mediated AMPAR endocytosis.

282 However, the mGluR-dependent reduction in ICa was not mimicked by Gbe

283 in-1 knock-out (KO) mice, application of the mGluR agonist, DHPG, did not result in B56alpha truncati

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

285 engages both mGluR1 and mGluR5 subtypes, the mGluR-dependent component of IPSCs elicited by intrastri

286 ecific agonists due to homologies within the mGluR family, and the Ca(2+)-binding site(s) on mGluR1al

287 Blockage of the mGluRs alone only modestly reduced the magnitude of the

288 Thus, mGluRs establish a local negative feedback loop position

289 responded with rapid changes in [Ca(2+)]i to mGluR agonists in a time-dependent fashion.

290 so, alcohol-dependent rats do not respond to mGluR(2/3) agonist treatment with reducing extracellular

291 also synthesized at synapses in response to mGluR activation.

292 tuned to l-amino acids, but variants of two mGluRs expressed in taste buds have also been implicated

293 ibe the translational program that underlies mGluR-LTD and identify the translation factor eIF2alpha

294 To determine whether mGluR activation can also induce LTP in the absence of N

295 This study sought to determine whether mGluR Copy Number Variants (CNV's) were overrepresented

296 To determine whether mGluR network CNV'S are enriched in syndromic ASD, we ex

297 work demonstrates a novel mechanism in which mGluR signals release AMPA receptors rapidly from the ER

298 omic ASD was more prevalent in children with mGluR CNVs (74% vs 16%, p < 0.001).

299 e spinal neurons that express MOR along with mGluRs and mERalpha, suggesting that signaling mechanism

300 e some signaling pathways and cooperate with mGluRs in the control of neuronal excitability.We theref