ライフサイエンスコーパス: mGluR5

1 d group I metabotropic glutamate receptor 5 (mGluR5).

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

3 stream of metabotropic glutamate receptor 5 (mGluR5).

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

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

6 cerebral metabotropic glutamate receptor 5 (mGluR5).

7 inding to metabotropic glutamate receptor 5 (mGluR5).

8 s of metabotropic glutamate receptor type 5 (mGluR5).

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

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

11 s acutely corrected by antagonizing striatal mGluR5.

12 tabotropic glutamate receptor 1 (mGluR1) and mGluR5.

13 stroglial metabotropic glutamate receptor 5 (mGluR5), a major receptor in mediating developmental ast

14 Septal deletion of mGluR5 abolished sociability while leaving preference fo

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

16 ties or downstream consequences of astrocyte mGluR5 activation during epilepsy development.

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

18 Type 1 mGluR5 activation increases TRPA1 receptor agonist sensi

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

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

21 A selective mGluR5 activator (VU0360172) increased pyramidal output

22 Accordingly, enhancing mGluR5 activity acutely recapitulates these behavioral p

23 horylation can be precipitated by attenuated mGluR5 activity and that increased mGluR5 phosphorylatio

24 Manipulation of mGluR5 activity attenuates excessive grooming and instru

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

26 findings uncover the role of the persistent mGluR5 activity in vivo and provide new insight into how

27 The decline of mGluR5 activity induced the pain modulatory dysfunction

28 early gene product, disrupted the persistent mGluR5 activity resulting in chronic pain.

29 hosphorylation of mGluR5, which can decrease mGluR5 activity via desensitization (p < 0.01).

30 reso 1 and tamalin, which can also attenuate mGluR5 activity.

31 ls frequently contacted dendrites containing mGluR5 adjacent to unlabeled terminals forming excitator

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

33 ding depotentiation, whereas infusion of the mGluR5 agonist CHPG itself promoted reinstatement and de

34 henotype that could be blocked with systemic mGluR5 allosteric antagonism via MTEP.

35 a radioligand that binds specifically to the mGluR5 allosteric site.

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 increased NMDA receptor gating, dependent on mGluR5 and linked to enhanced Ca(2+) influx.

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

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

41 h mGluR5, and the dynamic cross talk between mGluR5 and VGLUT3 is key for the function of specific ne

42 ptors and metabotropic glutamate receptor 5 (mGluR5) and assessed decision making using a probabilist

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

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

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

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

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

48 n overlapping, but unique, distribution with mGluR5, and the dynamic cross talk between mGluR5 and VG

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

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

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

52 Intra-NAc shell infusion of the mGluR5 antagonist MTEP blocked cocaine-primed reinstatem

53 3 knockout (KO) mice treated acutely with an mGluR5 antagonist were evaluated for OCD-relevant phenot

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

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

56 has been a problem with other drug classes (mGluR5 antagonists, GABA-A and -B agonists).

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

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

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

60 That mammalian GLT1 and mGluR5 are implicated in pathological motor repetition s

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

62 Findings point to the potential role for mGluR5 as a target for intervention and, potentially, su

63 r glutamate, supporting a potential role for mGluR5 as therapeutic target in human MTLE.

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

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

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

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

68 re, we tested whether the state of decreased mGluR5 availability in alcohol-dependent patients normal

69 Conclusion: Reduced cerebral mGluR5 availability in alcohol-dependent patients recove

70 Higher striatal mGluR5 availability in alcohol-dependent users may be as

71 ependent patients showed sustained recovered mGluR5 availability in cortical and subcortical regions

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

73 e (EZ), we characterized in vivo whole-brain mGluR5 availability in MTLE patients using positron emis

74 We observed significantly higher mGluR5 availability in PTSD compared with HC individuals

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

76 Focally reduced mGluR5 availability in the EZ might reflect receptor int

77 Importantly, we observed an up-regulation in mGluR5 availability in the PTSD-SI group (P's = 0.001-0.

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

79 on tomography and [(18)F]FPEB, we quantified mGluR5 availability in vivo in individuals with PTSD (n

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

81 mGluR5 availability was not significantly different betw

82 Higher striatopallidal mGluR5 availability was observed at the baseline in pati

83 mGluR5 availability was quantified by the (18)F-FPEB tot

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

85 No differences in mGluR5 availability, responses during tests of extinctio

86 hronic alcohol use leads to decreased limbic mGluR5 availability, which was associated with less crav

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

88 Pathological signaling of the VGLUT3-mGluR5 axis is linked to Parkinson disease, anxiety diso

89 Thus, aberrant signaling of the VGLUT3-mGluR5 axis is linked to various pathologies including,

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

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

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

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

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

95 and mGluR5, which was further supported for mGluR5 by immunolabeling results.

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

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

98 Deoxycholate (DOC), while Shank-, Homer- and mGluR5-containing interactions are more abundant in 1% N

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

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

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

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

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

104 Therefore, VGLUT3-mGluR5 cross talk can significantly influence both physi

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

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

107 during epileptogenesis, astrocytes reacquire mGluR5-dependent calcium transients following agonist ap

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

109 ndritic protein synthesis yields exaggerated mGluR5-dependent long-term synaptic depression (LTD) in

110 t is able to restore both NMDA-dependent and mGluR5-dependent LTD in animals after cocaine self-admin

111 mGluR5-dependent processes during early postnatal brain

112 Furthermore, reinstatement was driven by an mGluR5-dependent reduction in AMPAR signaling.

113 We found that mGluR5 depletion in VMH SF1 neurons did not affect energ

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

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

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

117 ing and reversals require EGL-30/Galphaq, an mGluR5 effector.

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

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

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

121 ehavior require the glutamate receptor MGL-2/mGluR5, expressed in RIM and other interneurons presynap

122 However, mGluR5 expression and function are transient in animals

123 Herein, we demonstrate that mGluR5 expression and function dramatically increase in

124 Perturbing mGluR5 expression could lead to abnormal neuronal circui

125 onditions, a feature that suggests astrocyte mGluR5 expression during epileptogenesis may recapitulat

126 In the rodent brain, astrocyte mGluR5 expression is developmentally regulated and confi

127 After early development, astrocyte mGluR5 expression is downregulated, but reemerges in ani

128 ent time period, suggesting that patterns of mGluR5 expression may signify continuing epilepsy develo

129 c interaction between tDCS and pharmacologic mGluR5 facilitation.

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

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

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

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

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

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

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

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

138 Interestingly, in both male and female mice, mGluR5 function persists in the astrocyte throughout the

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

140 ent astroglia sufficiently rescues decreased mGluR5 function, while astroglial overexpression of miR-

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

142 estingly, the patient group showed decreased mGluR5-GluN association (p < 0.01), a mechanistic basis

143 and suggest protein-protein interactions in mGluR5-GluN complexes as potential targets for intervent

144 Our results suggest a novel role of mGluR5-H1a interaction in strengthening contralateral ey

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

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

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

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

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

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

151 um, we present the first direct evidence for mGluR5 hypoactivity, propose a reciprocal interplay betw

152 6 mo of detoxification) and whether initial mGluR5 imaging parameters can predict individual relapse

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

154 we demonstrated here that knock-out (KO) of mGluR5 in cholinergic, but not glutamatergic or parvalbu

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

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

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

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

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

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

161 a novel role of H1a and its interaction with mGluR5 in strengthening contralateral eye inputs during

162 characterize the involvement of the receptor mGluR5 in the fine-tuning of NMDA receptors, specificall

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

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

165 We evaluated the importance of knocking-out mGluR5 in three different cell types in two brain region

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

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

168 on of metabotropic glutamatergic receptor 5 (mGluR5) in pathophysiology of PTSD and suicidality.

169 that the metabotropic glutamate receptor 5 (mGluR5) in the periaqueductal gray (PAG), the key area o

170 f metabotropic glutamate receptor subtype 5 (mGluR5) in the VMH is regulated by caloric status in nor

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

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

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

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

175 Spinal mGluR5 is a key mediator of neuroplasticity underlying p

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

177 mGluR5 is also trafficked to the plasma membrane where i

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

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

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

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

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

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

190 ession of metabotropic glutamate receptor 5 (mGluR5) is consistently observed in resected tissue from

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

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

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

194 cholinergic neurons of the medial septum in mGluR5 KO mice.

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 metric synapses are the likely source of the mGluR5 ligand glutamate.

198 Our findings elucidate a novel mGluR5-linked signaling state within BNST that plays a c

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

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

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

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

205 These data support a model in which mGluR5-mediated reduction in GluA2-containing AMPARs at

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

207 erstand the synaptic structure that supports mGluR5 mediation of CB1 activation in the prefrontal cor

208 gand-dependent internalization of mGluR1 and mGluR5, members of the group I mGluR family.

209 These findings led us to investigate whether mGluR5 might act downstream of BDNF to critically regula

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

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

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

213 regional cortical excitability referable to mGluR5-mTOR signaling.

214 asic phenotype of H1aKO was recapitulated by mGluR5 mutation that severely reduces H1a interaction.

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

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

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

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

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

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

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

227 This A(2A)R/mGluR5/NMDAR interaction might prove a suitable alternat

228 suitable alternative for regulating aberrant mGluR5/NMDAR signaling in AD without disrupting their co

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 pose a reciprocal interplay between GluN and mGluR5 pathways as integral to glutamatergic dysregulati

237 ttenuated mGluR5 activity and that increased mGluR5 phosphorylation can result from decreased GluN fu

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

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

240 mGluR5 presents a different organization and is homogeno

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

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

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

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

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

246 g in response to stimulation of postsynaptic mGluR5 receptors and facilitation of heterosynaptic comm

247 Activation of mGluR5 receptors enhances FMRP synthesis.

248 In it, glutamate signaling activates mGluR5 receptors to promote Ckd5-mediated phosphorylatio

249 in female hamsters depends on activation of mGluR5 receptors.

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

251 We explored the hypothesis that astrocyte mGluR5 reemergence recapitulates earlier developmental r

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

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

254 d metabotropic glutamate receptor subtype 5 (mGluR5) represents one such candidate.

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

256 Remarkably a single-time blockage of the mGluR5 resulted in chronic neuropathic pain-like symptom

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

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

259 Our work demonstrates that astrocytes with mGluR5 signaling during TLE development perform faster g

260 t the selective and conditional knock-out of mGluR5 signaling from astrocytes during epilepsy develop

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

262 g a previously unexplored role for astrocyte mGluR5 signaling in hypersynchronous pathology.

263 orylation) and here we show those of reduced mGluR5 signaling in schizophrenia.

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

265 We examined agonist-induced mGluR5 signaling in the postmortem dorsolateral prefront

266 ehensive profiling of how coordinated VGLUT3-mGluR5 signaling influences overall glutamatergic neurot

267 Notably, mGluR5 signaling is a positive regulator of astrocyte gl

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

269 Given these crucial roles, mGluR5 signaling is under the tight control of glutamate

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

271 IFICANCE STATEMENT In development, astrocyte mGluR5 signaling plays a critical role in regulating str

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

273 Excessive mGluR5 signaling underlies OCD-like behaviors and striat

274 patient group showed a striking reduction in mGluR5 signaling, manifested by decreases in Gq/11 coupl

275 selectively alters developmental astroglial mGluR5 signaling, unveiling astroglial molecular mechani

276 ectively diminishes developmental astroglial mGluR5 signaling.

277 eep loss-induced modifications downstream of mGluR5 signaling.

278 ing is reciprocal interplay between GluN and mGluR5 signaling.

279 n of metabotropic glutamate receptor type 5 (mGluR5) signaling and that this astrocyte-mediated respo

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

281 Blocking the astrocytic mGluR5-signaling pathway suppressed mechanical allodynia

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

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

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

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

286 exploration and the continued development of mGluR5 therapies.

287 Also, normalization of striatal mGluR5 to control levels was associated with reduced cra

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

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

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

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

292 postsynaptic metabotropic glutamate receptor mGluR5 triggers retrograde signaling of endocannabinoids

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

294 es in serine and tyrosine phosphorylation of mGluR5, which can decrease mGluR5 activity via desensiti

295 nce indicated involvement of both mGluR1 and mGluR5, which was further supported for mGluR5 by immuno

296 ow efficient optical control of G(q)-coupled mGluR5, which we use to probe the spatiotemporal propert

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

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

299 se from disrupted functional interactions of mGluR5 with estrogen receptors that switch the normally

300 altered protein-protein interaction (PPI) of mGluR5 with RGS4, norbin, Preso 1 and tamalin, which can