ライフサイエンスコーパス: mGluR

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

2 mGluR trafficking not only plays important roles in cont

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

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

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

6 Here, we identified a novel Group 1 mGluR-dependent mechanism that causes bidirectional, lon

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

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

9 other glutamated substrates, which activate mGluR I.

10 Activated mGluR I subsequently induces activation of phosphoinosit

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

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

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

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

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

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

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

18 synapses, how endogenous AMPARs, NMDARs, and mGluRs are co-organized inside the synapse and their res

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

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

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

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

23 cAMP levels can be regulated by mGluR signaling.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

45 term depression, consistent with facilitated mGluR-dependent activation.

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

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

48 ss believed to be the cellular correlate for mGluR-dependent synaptic plasticity.

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

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

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

52 ly, exposure of mice to loud sound caused G1 mGluR-dependent Z-LTD at DCN parallel fiber synapses, th

53 e receptors (G1 mGluRs) demonstrated that G1 mGluR activation is necessary and sufficient for inducin

54 Group 1 metabotropic glutamate receptors (G1 mGluRs) demonstrated that G1 mGluR activation is necessa

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

56 Dysregulated Gp1 mGluR signaling has been observed in numerous neurologic

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

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

59 ubiquitination and down-regulation upon Gp1 mGluR activation.

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

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

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

63 Group I metabotropic glutamate receptor (GpI mGluR) signaling to protein translation, we find that Gp

64 ing to protein translation, we find that GpI mGluR stimulation results in increased Cav2.3 translatio

65 nder basal conditions and in response to GpI mGluR stimulation.

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

67 11.5% of ASD had mGluR CNV's vs. 3.2% in controls (p < 0.001).

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

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

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

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

72 ull-length receptors, it remains unclear how mGluR activation proceeds at the level of the transmembr

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

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

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

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

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

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

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

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

81 awal, AIE altered LTD induced by the group I mGluR antagonist DHPG in females, but not males.

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

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

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

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

86 of mGluR1 and mGluR5, members of the group I mGluR family.

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

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

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

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

91 ng is lost, while CB1R-dependent and group I mGluR-dependent regulation are intact.

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

93 This work also assessed whether BNST group I mGluR-mediated long-term depression (LTD) was disrupted

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

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

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

97 the mechanisms of the modulation by group I mGluRs (mGluR Is) on spontaneous glutamate release in th

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

99 alin has been shown to interact with group I mGluRs and also with many other proteins involved in pro

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 ole of tamalin in the trafficking of group I mGluRs and suggest its physiological implications in the

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

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

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

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

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

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

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

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

115 ent inhibition via the activation of group I mGluRs.

116 erminal PDZ binding motif encoded by Group I mGluRs.

117 ail and second intracellular loop of Group I mGluRs.

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

119 isms that control the trafficking of group I mGluRs.

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

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

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

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

124 of excitatory synaptic terminals to group II mGluR agonist.

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

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

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

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

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

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

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

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

133 mit photo-agonism of G(i/o)-coupled group II mGluRs with near-complete efficiency relative to glutama

134 mechanism of full-length mammalian group II mGluRs.

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

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

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

138 eport that ELFN2 critically alters group III mGluR secondary messenger signaling by directly altering

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

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

141 in the selective downregulation of group III mGluRs and dysregulated glutamatergic synaptic transmiss

142 cardinal organizational feature of group III mGluRs essential for their signaling properties and brai

143 by pharmacological augmentation of group III mGluRs.

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

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

146 through indirectly stimulating group II/III mGluRs.

147 he canonical "autoreceptor" role of Type III mGluRs, and substantially altering synaptic pharmacology

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

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

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

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

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

153 0% with 22q11.2DS + ASD had "second hits" in mGluR network genes vs 2% in 22q11.2DS-ASD (p < 0.014).

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

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

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

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

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

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

160 strate that tamalin plays a critical role in mGluR-mediated internalization of alpha-amino-3-hydroxy-

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

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

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

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

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

166 Mechanistically, mGluR activation induced mRNA translation-dependent incr

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

168 hanisms of the modulation by group I mGluRs (mGluR Is) on spontaneous glutamate release in the medial

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

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

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

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

173 Activation of mGluR I by 3,5-dihydroxyphenylglycine (3,5-DHPG; 200 mum

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

175 onally modulates the surface availability of mGluR(5) and produces alterations in dendritic complexit

176 s reveal that the structural consequences of mGluR and metabotropic NMDAR activation differ, and that

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

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

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

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

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

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

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

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

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

186 memory formation required the activation of mGluRs instead of NMDARs.

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

188 tructure during LTD induced by activation of mGluRs or NMDA receptors (NMDARs), and how this plastici

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

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

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

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

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

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

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

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

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

198 and negative allosteric modulators (NAMs) of mGluRs.

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

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

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

202 nM), and excellent selectivity against other mGluR subtypes (>100-fold).

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

204 pparent affinity ~4000-fold lower than other mGluRs and a maximal activation of only ~10%, seemingly

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

206 Metabotropic glutamate receptor (mGluR) 5 exhibits promising therapeutic potential for ma

207 erlaps with metabotropic glutamate receptor (mGluR) 5 in regional brain circuitries, including striat

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

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

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

211 emories via metabotropic glutamate receptor (mGluR) activation.

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

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

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

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

216 erations in metabotropic glutamate receptor (mGluR) signalling.

217 response to metabotropic glutamate receptor (mGluR) stimulation, but the proteins expressed differ un

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

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

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

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

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

223 lly via the metabotropic glutamate receptor (mGluR).

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

225 Group I metabotropic glutamate receptors (mGluR) are a target of interest due to their regulation

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

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

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

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

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

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

232 ch include metabotropic glutamate receptors (mGluRs) and gamma-aminobutyric acid B (GABA(B)) receptor

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

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

235 Metabotropic glutamate receptors (mGluRs) are class C, synaptic G-protein-coupled receptor

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

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

238 Metabotropic glutamate receptors (mGluRs) are dimeric G-protein-coupled receptors that ope

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

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

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

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

243 e modes by metabotropic glutamate receptors (mGluRs) constitutes critical supporting evidence.

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

245 Metabotropic glutamate receptors (mGluRs) function as dimers.

246 group III metabotropic glutamate receptors (mGluRs) in trans.

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

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

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

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

251 Group I metabotropic glutamate receptors (mGluRs) play important roles in various neuronal functio

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

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

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

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

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

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

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

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

260 to target metabotropic glutamate receptors (mGluRs).

261 as type I metabotropic glutamate receptors (mGluRs).

262 lized with metabotropic glutamate receptors (mGluRs).

263 ight-gated metabotropic glutamate receptors (mGluRs).

264 ynapses by metabotropic glutamate receptors (mGluRs).

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

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

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

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

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

270 agonist activity at mGlu2 over the remaining mGluR subtypes.

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

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

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

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

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

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

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

278 We were surprised to find that mGluR activation causes LTD and AMPA receptor internaliz

279 Our data indicate that mGluR I enhances spontaneous glutamate release via regul

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

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

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

283 DHPG [(RS)-3,5-dihydroxyphenylglycine], the mGluR(1,5) agonist that targets F2 terminals.

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

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

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

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

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

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

290 Thus, mGluRs establish a local negative feedback loop position

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

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