ライフサイエンスコーパス: mGluR5

1 BDNF) and metabotropic glutamate receptor 5 (mGluR5).

2 aling via metabotropic glutamate receptor 5 (mGluR5).

3 c tail of metabotropic glutamate receptor 5 (mGluR5).

4 e metabotropic glutamate receptor subtype 5 (mGluR5).

5 P(C)) and metabotropic glutamate receptor 5 (mGluR5).

6 stream of metabotropic glutamate receptor 5 (mGluR5).

7 le of the metabotropic glutamate receptor 5 (mGluR5).

8 s acutely corrected by antagonizing striatal mGluR5.

9 ation of NMDA receptors (NMDARs) rather than mGluR5.

10 o acids 91-153 mediates the interaction with mGluR5.

11 ays that is critically modulated by striatal mGluR5.

12 luR2/3 blockade was not affected by blocking mGluR5.

13 ) increase in neurons via the complex PrP(C)-mGluR5.

14 more, a single dose of mGluR1 (0.3 mg/kg) or mGluR5 (3 mg/kg) antagonists in vivo reversed the defici

15 ation with either an mGluR1 (LY367385) or an mGluR5 (3-[(2-methyl-4-thiazolyl)ethynyl]pyridine) antag

16 and that pharmacological block of mGluR1 or mGluR5 abolished MF-LTP.

17 Septal deletion of mGluR5 abolished sociability while leaving preference fo

18 Using NO-sensitive electrodes, mGluR5 activation by glutamate was shown to stimulate NO

19 groundbreaking discovery that intracellular mGluR5 activation drives unique signaling pathways, incl

20 In an arthritis pain model mGluR5 activation failed to overcome abnormal synaptic i

21 Type 1 mGluR5 activation increases TRPA1 receptor agonist sensi

22 The immediate impact of mGluR5 activation is to produce anxiety manifested as in

23 The present study examined the effects of mGluR5 activation on extinction of ethanol-cue-maintaine

24 Restoring endocannabinoid signaling allows mGluR5 activation to increase infralimbic output hence i

25 ted CA1 neurons; however, only intracellular mGluR5 activation triggered sustained high amplitude Ca(

26 A selective mGluR5 activator (VU0360172) increased pyramidal output

27 Accordingly, enhancing mGluR5 activity acutely recapitulates these behavioral p

28 Manipulation of mGluR5 activity attenuates excessive grooming and instru

29 constitutive signaling to increased striatal mGluR5 activity in Sapap3 KO mice was investigated using

30 h and CREB phosphorylation were dependent on mGluR5 activity since MPEP normalized both responses.

31 dulators of mGluR5 do not alter Glu or basal mGluR5 activity, but they disrupt the Abetao-induced int

32 Activating BDNF or mGluR5 after training rescues the infantile amnesia.

33 roxyphenyl)acetic acid sodium salt (CHPG) an mGluR5 agonist restored sensitivity to alcohol in discri

34 Whereas p11 overexpression potentiates mGluR5 agonist-induced calcium responses, overexpression

35 Finally, activation of intracellular mGluR5 alone mediated both electrically induced and chem

36 n of metabotropic glutamate receptor subtype mGluR5 and endocannabinoid signaling in infralimbic pyra

37 ins that have a functional relationship with mGluR5 and glucocorticoids in PTSD.

38 y highly specialized roles of lateral septal mGluR5 and Oxtr in the the regulation of discrete social

39 istochemical analyses of the distribution of mGluR5 and Oxtr revealed non-overlapping localization of

40 An intra-CeA infusion of mGluR1, mGluR5 and PLC inhibitors all dose-dependently reduced b

41 The efficacy of mGluR1, mGluR5 and PLC inhibitors to reduce binge intake depende

42 were additive, whereas those of coinhibiting mGluR5 and PLC were not, indicating that the efficacy of

43 ity also increases the expression of nuclear mGluR5 and receptor-mediated phosphorylated-ERK1/2, Arc/

44 identified Norbin as a positive regulator of mGluR5 and showed that its expression promotes neurite o

45 amma1 promotes internalization of PrP(C) and mGluR5 and transiently decreases AbetaO biding to neuron

46 ated with metabotropic glutamate receptor 5 (mGluR5) and dopaminergic dysfunctions.

47 n-coupled metabotropic glutamate receptor 5 (mGluR5) and oxytocin receptor (Oxtr) affect social affil

48 vation of metabotropic glutamate receptor 5 (mGluR5) and protein synthesis in the NAc shell, but not

49 ment with metabotropic glutamate receptor 5 (mGluR5) and Src antagonists blocked the BMAA-induced inh

50 metabotropic glutamate receptors (mGluR1 and mGluR5) and their relevance to the hyperactivity of PVN

51 ally with metabotropic glutamate receptor 5 (mGluR5), and this interaction controls the transmission

52 KO) that metabotropic glutamate receptor 5 (mGluR5)- and protein-synthesis-dependent synaptic plasti

53 However, adult astrocytes lack mGluR5, and knockout of the inositol 1,4,5-trisphosphate

54 [(18)F]FPEB, a radioligand that binds to the mGluR5, and positron emission tomography (PET) to quanti

55 nzonitrile), a selective PET radioligand for mGluR5, and used it to quantify mGluR5 in rat brain.

56 We found that mGluR5- and protein-synthesis-dependent synaptic plastic

57 tify a molecular and cellular basis by which mGluR5 antagonism achieves its antidepressant-like activ

58 EAAT-3, mimics the effects of intracellular mGluR5 antagonism.

59 ion was blocked by the local infusion of the mGluR5 antagonist 3-((2-methyl-4-thiazolyl)ethynyl) pyri

60 refore, we tested whether treatment with the mGluR5 antagonist MPEP normalizes synaptic and learning

61 In one experiment, local infusion of the mGluR5 antagonist MTEP in the DA-denervated rat striatum

62 t ligands that contain mu opioid agonist and mGluR5 antagonist pharmacophores linked through spacers

63 3 knockout (KO) mice treated acutely with an mGluR5 antagonist were evaluated for OCD-relevant phenot

64 t with the candidate therapeutic fenobam, an mGluR5 antagonist.

65 with the metabotropic glutamate receptor 5 (mGluR5) antagonist 2-methyl-6-(phenylethynyl)-pyridine.

66 rease the mGluR5-PrP(C) interaction, whereas mGluR5 antagonists suppress protein association.

67 inhibited sexual motivation but mGluR2/3 and mGluR5 antagonists were ineffective.

68 Eif4ebp2(-/-) mice was rescued by mGluR1 or mGluR5 antagonists.

69 Although mGluR5-antagonists prevent fear and anxiety, little is k

70 PrP(C) and mGluR5 are co-receptors also for beta-amyloid oligomers

71 ior and strongly support further research on mGluR5 as a potential therapeutic target in neuropsychia

72 ways, laminin-PrP(C)-mGluR5 or AbetaO-PrP(C)-mGluR5, as well as their interplay.

73 a significant ketamine-induced reduction in mGluR5 availability (that is, [(11)C]ABP688 binding) in

74 halography in humans, we find that increased mGluR5 availability after sleep loss tightly correlates

75 SD in vivo and positive correlations between mGluR5 availability and avoidance symptoms.

76 cocaine use is associated with a decrease in mGluR5 availability compared with matched healthy contro

77 mission tomography (PET) to quantify in vivo mGluR5 availability in human PTSD vs. healthy control (H

78 We observed significantly higher cortical mGluR5 availability in PTSD in vivo and positive correla

79 ament was robustly associated with increased mGluR5 availability in various regions including the tha

80 otransmission, we hypothesized that cerebral mGluR5 availability is associated with temperament trait

81 Brain mGluR5 availability was quantified on both a voxel-by-vo

82 ased after ketamine administration moderates mGluR5 availability; this change appears to be related t

83 adiotracer [(11)C]ABP688 was used to measure mGluR5 binding and magnetic resonance spectroscopy was u

84 years), and to explore associations between mGluR5 binding and relapse in recent ex-smokers.

85 ho had never smoked showed no differences in mGluR5 binding in any of the brain regions examined.

86 -term ex-smokers showed significantly higher mGluR5 binding than recent ex-smokers, most prominently

87 s in metabotropic glutamate receptor type 5 (mGluR5) binding in smokers and recent ex-smokers (averag

88 iatum, CA1 neurons exhibited an abundance of mGluR5 both on the cell surface and intracellular membra

89 gical approach to isolate different pools of mGluR5, both intracellular and cell surface receptors in

90 and QRT-PCR analysis showed that astroglial mGluR5 (but not GLT1) mRNA is associated with FMRP.

91 luR2/3 blockade was reversed by antagonizing mGluR5, but reinstated sucrose seeking in the absence of

92 Consistent with the notion that mGluR5 can signal from intracellular membranes, uncaging

93 rs the physiological signaling of the PrP(C)-mGluR5 complex upon glutamate activation.

94 We propose that targeting the PrP(C)-mGluR5 complex will reverse aberrant Abetao-triggered st

95 The data suggest that mGluR5 contribute to the brain's coping mechanisms with

96 tabotropic glutamate receptors of subtype 5 (mGluR5) contribute to the molecular machinery governing

97 The results support the hypothesis that mGluR5 coordinates a reduction in mGluR1 functional acti

98 We demonstrate that inhibition of mGluR5 corrects hyperactivity, seizures, and elevated de

99 estion whether inhibition or potentiation of mGluR5 could be beneficial depends, among other factors,

100 tiating a metabotropic glutamate receptor 5 (mGluR5)-dependent increase in nitric oxide (NO) producti

101 ound that metabotropic glutamate receptor 5 (mGluR5)-dependent synaptic plasticity and protein synthe

102 us, Abetao triggers multiple distinct PrP(C)-mGluR5-dependent events implicated in neurodegeneration

103 ding dendritic spine abnormalities, abnormal mGluR5-dependent LTD, as well as aberrant behaviors in o

104 mGluR5-dependent processes during early postnatal brain

105 ed suppression of synaptic transmission from mGluR5-dependent to mGluR1-dependent.

106 g seeking by activating nNOS, but activating mGluR5 did not promote reinstated sucrose seeking, nor w

107 clude the metabotropic glutamate receptor 5 (mGluR5), dipeptidyl-peptidase-like protein-6 (DPPX), and

108 eraction of PrP(C) and mGluR5 is reversed by mGluR5-directed antagonists or antibodies directed again

109 global reduction (20.6%; P < 0.0001) in the mGluR5 distribution volume ratio (DVR) in the gray matte

110 Silent allosteric modulators of mGluR5 do not alter Glu or basal mGluR5 activity, but th

111 cant mGluR5 modulation, the specific role of mGluR5 downregulation in ketamine's antidepressant respo

112 oal of this study was to examine the role of mGluR5 downregulation in nicotine addiction by investiga

113 eversed by positive allosteric modulation of mGluR5 during extinction training, an effect that is tho

114 global reductions in the average gray matter mGluR5 DVR (11.5%; P < 0.005), and there was a significa

115 ignificant difference in average gray matter mGluR5 DVR between smokers and ex-smokers (9.2%; P < 0.0

116 ate receptors (mGluRs), including mGluR1 and mGluR5, elicits translation-dependent neural plasticity

117 Spinophilin knock-out results in enhanced mGluR5 endocytosis as well as increased ERK1/2, AKT, and

118 Knock-out mice without functional mGluR5 exhibit severe dysregulation of sleep-wake homeos

119 In the accumbens, we found reduced mGluR5 expression (immunohistochemistry and Western blot

120 Perturbing mGluR5 expression could lead to abnormal neuronal circui

121 e in metabotropic glutamate receptor type 5 (mGluR5) expression and reduced glutamate turnover.

122 earning and demonstrate that manipulation of mGluR5 facilitates extinction of ethanol cues in associa

123 c interaction between tDCS and pharmacologic mGluR5 facilitation.

124 cept that metabotropic glutamate receptor 5 (mGluR5) fails to engage endocannabinoid (2-AG) signaling

125 using antagonists of mGluR1 (JNJ16259685) or mGluR5 (fenobam).

126 Here, we describe mGluR5 findings in stress disorders, particularly major

127 MeCP2-mediated transcription regulation and mGluR5/FMRP-mediated protein translation regulation thro

128 These results suggest that PrP(C)-mGluR5 form a functional response unit by which multiple

129 inin, and metabotropic glutamate receptor 5 (mGluR5) form a protein complex on the plasma membrane th

130 Deletion of mGluR5 from Pv(+) interneurons resulted in reduced numbe

131 rescue of impaired endocannabinoid-dependent mGluR5 function in the mPFC can restore mPFC output and

132 mGluR5 function was rescued by restoring 2-AG-CB1 signal

133 Finally, evidence for a similar mGluR1/mGluR5 functional dependence is shown in medium spiny st

134 utamatergic neurons receiving sensory input, mGluR5 genetic mosaic mice were generated through in ute

135 d that an existing complex containing PrP(C)-mGluR5 has an important role in AbetaO binding and activ

136 molecules, whereas blockade of cell-surface mGluR5 has little effect.

137 on of the signal transduction from PrP(C) to mGluR5 has therapeutic potential for AD, we developed as

138 (NAM) of metabotropic glutamate receptor 5 (mGluR5) have been implicated as a potential pharmacother

139 targeting metabotropic glutamate receptor 5 (mGluR5) have therapeutic potential in autism spectrum di

140 gs show that deficiency of Shank3 can impair mGluR5-Homer scaffolding, resulting in cortico-striatal

141 Both mGluR5-Homer scaffolds and mGluR5-mediated signalling ar

142 cognitive deficit that is likely mediated by mGluR5/Homer1 signaling in the hippocampus.

143 ate cooperative signaling between mGluR1 and mGluR5 in a manner inconsistent with heterodimerization,

144 D, there has been much less investigation of mGluR5 in bipolar disorder, yet initial studies indicate

145 Conditional ablation of mGluR5 in CA1 pyramidal neurons resulted in the inabilit

146 bodies on the interaction between PrP(C) and mGluR5 in cell lines and mouse brain.

147 genic mice with a cell-specific knockdown of mGluR5 in D1 receptor-expressing neurons.

148 The role of striatal mGluR5 in D1-dependent ERK1/2 activation was confirmed i

149 the presence of opioid receptors (MORs) and mGluR5 in glia and neurons, together with reports that s

150 elevant and important role for intracellular mGluR5 in hippocampal synaptic plasticity.

151 Overall, these data posit mGluR5 in key paralimbic areas as a strong determinant o

152 l growth factor-related receptor) in PCD and mGluR5 in limbic encephalitis (LE).

153 tudies report either no differences or lower mGluR5 in MDD, potentially reflecting MDD heterogeneity.

154 Pharmacological stimulation of mGluR5 in NAcore recapitulated cue-induced reinstatement

155 eful tracer for in vivo visualization of the mGluR5 in rat brain.

156 ioligand for mGluR5, and used it to quantify mGluR5 in rat brain.

157 Combining in vitro and in vivo activation of mGluR5 in rats, we identify specific changes in intrinsi

158 impact of the CORT-induced downregulation of mGluR5 in relation to sensitivity to alcohol.

159 Our findings suggest a fundamental role for mGluR5 in the development of Pv(+) neurons and show that

160 The mRNA and protein levels of mGluR5 in the PVN and rostral ventrolateral medulla were

161 Our findings suggest that mGluR5 in the PVN is upregulated in hypertension and con

162 The role of mGluR5 in the striatal circuit abnormalities of Sapap3 K

163 gh there is evidence for the upregulation of mGluR5 in these disorders.

164 opic glutamate receptors (mGluRs, especially mGluR5) in developing cortical astroglia and found that

165 ng to a metabotropic glutamatergic receptor (mGluR5) in individuals with major depressive disorder (M

166 Deleting metabotropic glutamate receptor 5 (mGluR5) in mice perturbs cortical somatosensory map form

167 metabotropic glutamate receptors-subtype 5 (mGluR5) in the nucleus accumbens, as these receptors in

168 Agonists of mGluR5 increase the mGluR5-PrP(C) interaction, whereas m

169 While rescue by mGluR5 inhibition occurs through the blockade of a prote

170 ce to OCD and show the tractability of acute mGluR5 inhibition to remedy circuit and behavioral abnor

171 (LTD) leading to several clinical trials of mGluR5 inhibitors/modulators, yet all have failed.

172 t a membrane-permeable peptide that disrupts mGluR5 interactions with long-form Homers enhanced mGluR

173 ed decrease in binding may reflect prolonged mGluR5 internalization in response to the glutamate surg

174 Spinal mGluR5 is a key mediator of neuroplasticity underlying p

175 Our findings suggest that downregulation of mGluR5 is a pathogenetic mechanism underlying nicotine d

176 mGluR5 is also trafficked to the plasma membrane where i

177 ntive evidence that the inhibition of mGluR1/mGluR5 is an effective treatment for physiological and b

178 Given that mGluR5 is critical for toxic signaling by AbetaOs and in

179 The interaction of PrP(C) and mGluR5 is enhanced dramatically in the brains of familia

180 r physiological role of spinal intracellular mGluR5 is established.

181 w that in spinal dorsal horn neurons >80% of mGluR5 is intracellular, of which approximately 60% is l

182 Although brain mGluR5 is localized on cell surface and intracellular me

183 Thus, mGluR5 is perfectly positioned to regulate nucleoplasmic

184 We found that mGluR5 is required for several key steps in wiring up th

185 Specifically, mGluR5 is required in cortical glutamatergic neurons for

186 s with Abetao, the interaction of PrP(C) and mGluR5 is reversed by mGluR5-directed antagonists or ant

187 ally, our data suggest that once at the INM, mGluR5 is stably retained via interactions with chromati

188 t metabotropic glutamate receptors (mGluRs), mGluR5 is the most highly expressed in neural stem cells

189 The metabotropic glutamate receptor 5 (mGluR5) is a high-interest target for PET imaging becaus

190 mple, the metabotropic glutamate receptor 5 (mGluR5) is concentrated at the inner nuclear membrane (I

191 d through metabotropic glutamate receptor 5 (mGluR5) is involved in the pathophysiology of Autism Spe

192 Metabotropic glutamate receptor 5 (mGluR5) is widely expressed throughout the CNS and parti

193 ng thalamocortical axon (TCA) clusters while mGluR5 knock-out (KO) neurons were placed in the septal

194 aOs and in prion diseases, we tested whether mGlur5 knock-out mice would be susceptible to prion infe

195 miniature excitatory postsynaptic events in mGluR5 KO neurons compared with neighboring wild-type ne

196 The dendritic spine density of mGluR5 KO spiny stellate neurons was significantly highe

197 d that BMAA treatment dissociated PP2Ac from mGluR5, making it available for phosphorylation at Tyr(3

198 These results suggest that activation of mGluR5 may alleviate the functional impact of the CORT-i

199 mechanisms underlying PTSD and suggest that mGluR5 may be a promising target for mechanism-based tre

200 We propose that trafficking of PrP(C)-mGluR5 may modulate signaling intensity by different PrP

201 Recent work suggests that mGluR1 and mGluR5 may physically interact, but the nature and funct

202 However, while antagonism of mGluR5 may reduce fear conditioning, it may also reduce

203 tabotropic glutamatergic receptor subtype 5 (mGluR5) may represent a promising therapeutic target for

204 ons, and it had no effect on the size of the mGluR5-mediated current.

205 ock-out mouse, has demonstrated an increased mGluR5-mediated long-term depression (LTD) leading to se

206 Priming-induced metaplasticity requires mGluR5-mediated mobilization of endocannabinoids during

207 bility, as well as facilitated glutamatergic mGluR5-mediated persistent firing, compared with sham ne

208 Both mGluR5-Homer scaffolds and mGluR5-mediated signalling are selectively altered in st

209 re, studies are needed to determine the role mGluR5 modulation might play in the treatment of these c

210 allosteric modulation or full antagonism) of mGluR5 modulation required to translate existing knowled

211 amine may work, in part, through significant mGluR5 modulation, the specific role of mGluR5 downregul

212 regional cortical excitability referable to mGluR5-mTOR signaling.

213 induced calcium responses, overexpression of mGluR5 mutant, which does not interact with p11, diminis

214 p11 and mGluR5 mutually facilitate their accumulation at the pla

215 ative and positive allosteric modulators (an mGluR5 NAM and PAM) for TSC, using a mutant mouse model

216 wed its nomination as a novel, nonacetylenic mGluR5 NAM clinical candidate.

217 Most of the mGluR5 NAM clinical candidates can be characterized by t

218 In Mecp2 KO mice, we found that mGluR5 NAM treatment significantly reduced the level of

219 aluated basimglurant, a potent and selective mGluR5 NAM, in a 12-week, double-blind, parallel-group s

220 y potent, selective, and orally bioavailable mGluR5 NAM.

221 ggest a meaningful therapeutic potential for mGluR5 NAMs in TSC, which warrants clinical exploration

222 The early short-term clinical trials with mGluR5 NAMs, including basimglurant, assessing the effec

223 DCS-LTD is abolished with an mGluR5 negative allosteric modulator, mechanistic target

224 of pyrazolopyrazines is herein disclosed as mGluR5 negative allosteric modulators (NAMs).

225 tegies, we tested the therapeutic utility of mGluR5 negative and positive allosteric modulators (an m

226 t chronic treatment of Mecp2 KO mice with an mGluR5-negative allosteric modulator tunes down upregula

227 Treatment of Fmr1 knockout mice with mGluR5-negative allosteric modulators (NAMs) has been re

228 In the Fmr1 KO mouse, chronic treatment with mGluR5-negative allosteric modulators (NAMs) has been sh

229 Manipulating the interaction between mGluR5, NO production, or MMP-2 and MMP-9 pharmacologica

230 metabotropic glutamate receptors, mGluR1 and mGluR5, occurs through G-protein coupling, but evidence

231 timulates metabotropic glutamate receptor 5 (mGluR5) on a small population of interneurons ( approxim

232 activate metabotropic glutamate receptor 5 (mGluR5) on astrocytes, evoking Ca(2+) release from inter

233 stimulate metabotropic glutamate receptor5 (mGluR5) on neuronal nitric oxide synthase (nNOS) interne

234 these two signaling pathways, laminin-PrP(C)-mGluR5 or AbetaO-PrP(C)-mGluR5, as well as their interpl

235 Conversely, knockout of mGluR5 or p11 in GABAergic neurons causes antidepressant

236 Knockout of mGluR5 or p11 specifically in glutamatergic neurons in m

237 ts in FMRP-deficient mice stem from elevated mGluR5 (or GRM5) function, similar to a subset of fragil

238 t of metabotropic glutamate receptor type 5 (mGluR5) or its downstream signaling molecules (PLC, PKC,

239 one that does not interact with the nuclear mGluR5 pool.

240 they were administered either vehicle or the mGluR5 positive allosteric modulator 3-cyano-N-(1,3-diph

241 iphenyl-1H-pyrazol-5-yl)benzamide (CDPPB) an mGluR5 positive allosteric modulator and the intra-accum

242 An mGluR5-positive allosteric modulator, in contrast, trans

243 R5, the consequent release of PP2Ac from the mGluR5-PP2A complex, and its phosphorylation at Tyr(307)

244 Agonists of mGluR5 increase the mGluR5-PrP(C) interaction, whereas mGluR5 antagonists su

245 Therefore, mGluR5 receptor binding appears to be an effective bioma

246 Images of mGluR5 receptor binding were acquired in 14 long-term ex

247 elation between cocaine-seeking behavior and mGluR5 receptor binding.

248 tergic signaling, mediated by the astroglial mGluR5 receptor, regulates the functional maturation of

249 in PSD-95 is prevented by antagonism of the mGluR5 receptor.

250 on of the metabotropic glutamate receptor 5 (mGluR5) receptor might hold therapeutic benefits in Frag

251 DAR-mediated signaling through antagonism of mGluR5 receptors (2-methyl-6-(phenylethynyl) pyridine (M

252 y treatment of the animals with a blocker of mGluR5 receptors (MPEP), cocaine no longer decreased the

253 er with reports that suggest coexpressed MOR/mGluR5 receptors in cultured cells associate as a hetero

254 in female hamsters depends on activation of mGluR5 receptors.

255 Spinal blockade of intracellular mGluR5 reduces neuropathic pain behaviours and signallin

256 Blockade of intracellular mGluR5 represents a new strategy for the development of

257 ally, the metabotropic glutamate receptor 5 (mGluR5) represents a promising treatment target.

258 mGluR1-mediated inhibition and restored the mGluR5 responsiveness to a state functionally similar to

259 Activation of mGluR1 and mGluR5 resulted in a mixture of inward and outward curre

260 onversely, positive allosteric modulation of mGluR5 results in the exacerbation of hyperactivity and

261 ment with a negative allosteric modulator of mGluR5 reversed the cognitive deficit.

262 opic glutamate receptors (mGluRs) mGluR1 and mGluR5 reverses the autistic phenotypes in several ASD m

263 etitive antagonist with either an mGluR1- or mGluR5-selective negative allosteric modulator (NAM) BAY

264 The data suggest that ongoing mGluR5 signaling during a critical period of postnatal d

265 ings demonstrate a causal role for increased mGluR5 signaling in driving striatal output abnormalitie

266 To examine the cell-autonomous influences of mGluR5 signaling in the morphological and functional dev

267 tivity, indicating that bifenthrin amplifies mGluR5 signaling independent of Na(+) channel modificati

268 In Sapap3 KO mice, elevated mGluR5 signaling is associated with constitutively activ

269 supporting the cell-autonomous influence of mGluR5 signaling on the functional and anatomical develo

270 rt that chronic postnatal down-regulation of mGluR5 signaling produces coordinated impairments in bot

271 d stimulate designer receptors that mimicked mGluR5 signaling through Gq in nNOS interneurons, we rec

272 Excessive mGluR5 signaling underlies OCD-like behaviors and striat

273 ein kinase pAkt, but independent of T1R3 and mGluR5 signaling.

274 ase, the stabilization phase, which requires mGluR5 signaling.

275 eep loss-induced modifications downstream of mGluR5 signaling.

276 immature metabotropic glutamate receptor 5 (mGluR5) signaling in S1 astroglia, which elicits spontan

277 Blocking the astrocytic mGluR5-signaling pathway suppressed mechanical allodynia

278 To determine whether mGluR5 signals from intracellular membranes of other cel

279 Here, we found that selectively blocking mGluR5 significantly reduced the basal firing activity o

280 rapidly acting glutamatergic agent ketamine, mGluR5-specific modulation has not yet shown antidepress

281 disorder, yet initial studies indicate that mGluR5-specific treatments may aid in both depressed and

282 f spinophilin expression results in impaired mGluR5-stimulated LTD.

283 In cocaine-trained rodents mGluR5 stimulation reinstates drug seeking by activating

284 The decline was regulated by T1R3 and mGluR5, suggesting a novel negative regulator pathway fo

285 by inhibiting PP2A through the activation of mGluR5, the consequent release of PP2Ac from the mGluR5-

286 In neurons expressing mGluR1 and mGluR5, the selective NAMs each strongly inhibited the r

287 exploration and the continued development of mGluR5 therapies.

288 Shank3 leads to an increased localization of mGluR5 to both synaptosome and postsynaptic density-enri

289 Finally, sufficiency of mGluR5 to drive OCD-like behavior in wild-type mice was

290 t restoring endocannabinoid signaling allows mGluR5 to increase mPFC output hence inhibit pain behavi

291 regulation of SHANK1, a protein that anchors mGluR5 to the cell surface, as well as decreased express

292 To facilitate the development of mGluR5 treatment strategies, we tested the therapeutic u

293 stance); via T1R3, it protected EBF, whereas mGluR5 was associated with EBF loss.

294 unctional interdependence between mGluR1 and mGluR5 was demonstrated.

295 Thus, the activation of mGluR5 was required for the cocaine-mediated suppression

296 which the metabotropic glutamate receptor 5 (mGluR5) was specifically ablated from Pv(+) interneurons

297 s that inhibit the interaction of PrP(C) and mGluR5, which plays a pivotal role in the pathogenesis o

298 in wild-type mice was tested by potentiating mGluR5 with a positive allosteric modulator.

299 Inhibition of mGluR5 with an antagonist, 2-methyl-6-(phenylethynyl)pyr

300 ey disrupt the Abetao-induced interaction of mGluR5 with PrP(C).