ライフサイエンスコーパス: mGluR1

1 e 1 metabotropic glutamate receptors (cL-LTP(mGluR1)).

2 gnaling in transcriptional control in cL-LTP(mGluR1).

3 used to record conformational changes in the mGluR1.

4 ain was bound specifically and reversibly to mGluR1.

5 gmental area (VTA) through the activation of mGluR1.

6 n reported in association with antibodies to mGluR1.

7 c acetylcholine receptor, or via coexpressed mGluR1.

8 w that CaM specifically binds mGluR5 and not mGluR1.

9 ucine is sufficient to confer CaM binding to mGluR1.

10 CPPHA is also a PAM at mGluR1.

11 required the metabotropic glutamate receptor mGluR1.

12 volved in the ligand-mediated endocytosis of mGluR1.

13 likely involves glutamate signaling through mGluR1.

14 Furthermore, a single dose of mGluR1 (0.3 mg/kg) or mGluR5 (3 mg/kg) antagonists in vi

15 Agonists for mGluR1/5 (DHPG) or mGluR5 (CHPG) increased neuronal exci

16 ly, cocaine-experienced rats infused with an mGluR1/5 agonist before the initial test for cocaine-see

17 e results, intra-shell microinjection of the mGluR1/5 agonist DHPG (250 mum) promoted cocaine seeking

18 nocifensive behaviors evoked by intrathecal mGluR1/5 agonist injection after the resolution of IL-6-

19 cked in WT neurons by addition of Glu or the mGluR1/5 agonist, dihydroxyphenylglycine, to the medium,

20 s, which are prominent anchoring proteins of mGluR1/5 and are highly expressed in the striatum and th

21 g in preCGG neurons, which is ameliorated by mGluR1/5 antagonists or augmentation of GABA(A) receptor

22 ne-experienced rats infused intra-vmPFC with mGluR1/5 antagonists, either before or after an initial

23 aveolin-1 in mGluR trafficking, we show that mGluR1/5 associate with lipid rafts in the brain and tha

24 Site(s) in the intracellular loops of mGluR1/5 directly bind caveolin-1, an adaptor protein th

25 ssociated with a time-dependent reduction in mGluR1/5 expression within ventromedial PFC (vmPFC) of c

26 Furthermore, Homer proteins regulate mGluR1/5 function by acting as adapters and facilitating

27 MRP and the signaling pathways downstream of mGluR1/5 have yielded deeper insight into how synaptic p

28 ngly, pharmacological manipulations of vmPFC mGluR1/5 produced no immediate effects on cue-induced co

29 e dose of the psychostimulant amphetamine on mGluR1/5 protein expression in the rat forebrain in vivo

30 utant males, unlike females, showed enlarged mGluR1/5 responses and accelerated spontaneous firing.

31 Thus, a definitive demonstration of mGluR1/5 signal regulation by natively expressed Homer p

32 These results demonstrate abnormal mGluR1/5 signaling in preCGG neurons, which is ameliorat

33 Dysregulation of mGluR1/5 signaling is implicated in some disorders of ne

34 oneurosomes is rapidly dephosphorylated upon mGluR1/5 stimulation, whereas it is phosphorylated in WT

35 aveolin-1 is required for normal coupling of mGluR1/5 to downstream signaling cascades and induction

36 of the metabotropic glutamate receptor 1/5 (mGluR1/5) agonist DHPG (dihydroxyphenylglycol) precipita

37 hile pressure ejection of the group I mGluR (mGluR1/5) agonist DHPG [(S)-3,5-dihydroxyphenylglycine]

38 Group I metabotropic glutamate receptors (mGluR1/5) are important to synaptic circuitry formation

39 in response to activation of group 1 mGluRs (mGluR1/5), TACE cleaves NPR and releases the pentraxin d

40 s with metabotropic glutamate receptors 1/5 (mGluR1/5).

41 mGluR1/5-dependent activation (phosphorylation) of MEK a

42 lls of males had smaller synaptically evoked mGluR1/5-dependent currents, slower Purkinje-mediated IP

43 tion in neurons abolishes its suppression on mGluR1/5-dependent dendritic protein translation, enhanc

44 This process is necessary for mGluR1/5-dependent LTD in hippocampal and cerebellar syn

45 ent dendritic protein translation, enhancing mGluR1/5-dependent synaptic plasticity and other disease

46 Together, our data indicate that mGluR1/5-mediated glutamatergic excitation of cholinergi

47 rom group I metabotropic glutamate receptors mGluR1/5.

48 tration of an mGluR5 (9.0 mum MPEP), but not mGluR1 (50.0 mum YM 298198), antagonist before a priming

49 The mGluR1 (7-(hydroxyimino)cyclopropa [b]chromen-1a-carboxy

50 esidue (Lys(1112)) at the C-terminal tail of mGluR1 (a member of the group I mGluR family) plays cruc

51 f the metabotropic glutamate receptor-1 (BBB-mGluR1), a widely abundant CNS target, or an IgG that do

52 2-amino-2-(3,5-dihydroxyphenyl) acetic acid (mGluR1)-activated TPRC3 current as for recombinant TRPC3

53 ritic OPHN1 synthesis, which is dependent on mGluR1 activation and independent of fragile X mental re

54 Our modeling suggests that low levels of mGluR1 activation on a background of mAChR agonists may

55 erred the EC(50) and frequency dependence of mGluR1 activation under non-steady-state conditions, as

56 Following mGluR1 activation, the native erg current was reduced by

57 ception by both the nature of the endogenous mGluR1 activator (i.e., endogenous biased agonism at mGl

58 cle, as well as the nature of the endogenous mGluR1 activator, could encourage noncanonical pharmacol

59 ither by high-frequency stimulation of PF or mGluR1 agonist DHPG, was prolonged in MAGL(-/-) mice.

60 In rat striatal neurons, the mGluR1 agonist triggers the receptor-associated phosphoi

61 mAChR) or metabotropic glutamate receptor 1 (mGluR1) agonists on thalamic reticular (RE), thalamocort

62 ot displace binding of a radioligand for the mGluR1 allosteric antagonist characterized previously.

63 ible relationship to metabotropic glutamate (mGluR1 alpha and 5) and TrkB receptors which interact wi

64 In addition, Cd, Cp, mGluR1 alpha and cortical afferents are co-distributed i

65 mGluR1 alpha and TrkB immunoreactivities were invariably

66 with Cd and Cp-immunoreactive spines whereas mGluR1 alpha IR and mGluR5 IR were almost exclusively as

67 PPHA acts at a novel allosteric site on both mGluR1 and -5 to potentiate responses to activation of t

68 or mGluR2, it acts as a weak antagonist for mGluR1 and a potent antagonist for mGluR2, suggesting th

69 r phenotype that manifests in mutants of the mGluR1 and GluRdelta2 signaling pathways.

70 Activation of the metabotropic receptor mGluR1 and inhibition of I(h) channels caused a majority

71 Coimmunoprecipitation showed that ERalpha-mGluR1 and mGluR1-IP3R complexes exist in both sexes but

72 By contrast, in cells coexpressing mGluR1 and mGluR2, combining the same mGluR1 competitive

73 identify residues that when swapped between mGluR1 and mGluR4 increased the potency of L-SOP inhibit

74 data demonstrate differential sensitivity of mGluR1 and mGluR5 expression to amphetamine.

75 ta demonstrate cooperative signaling between mGluR1 and mGluR5 in a manner inconsistent with heterodi

76 nding, we examined the surface expression of mGluR1 and mGluR5 in hippocampal neurons.

77 Although it has been accepted that both mGluR1 and mGluR5 interact with CaM, we now show that Ca

78 Recent work suggests that mGluR1 and mGluR5 may physically interact, but the natur

79 trafficking and signaling, and distinguishes mGluR1 and mGluR5 regulation.

80 Activation of mGluR1 and mGluR5 resulted in a mixture of inward and ou

81 I metabotropic glutamate receptors (mGluRs) mGluR1 and mGluR5 reverses the autistic phenotypes in se

82 isoforms can act as a switch to reprioritize mGluR1 and mGluR5 signaling at the point of IP(3) recept

83 Group I mGluRs (mGluR1 and mGluR5 subtypes) are expressed in striatal me

84 dihydroxyphenylglycine] equally engages both mGluR1 and mGluR5 subtypes, the mGluR-dependent componen

85 vation, a functional interdependence between mGluR1 and mGluR5 was demonstrated.

86 pheneacetic acid) plus MPEP, as long as both mGluR1 and mGluR5 were blocked.

87 I metabotropic glutamate receptors (subtypes mGluR1 and mGluR5) and activation of protein kinase C (P

88 in group I metabotropic glutamate receptors (mGluR1 and mGluR5) and their relevance to the hyperactiv

89 Group I metabotropic glutamate receptors (mGluR1 and mGluR5) are important neuronal mediators of p

90 Group 1 mGluRs (mGluR1 and mGluR5) are primarily coupled to Galpha(q/11)

91 The group I mGluRs (mGluR1 and mGluR5) have long intracellular C-terminal do

92 of group I metabotropic glutamate receptors (mGluR1 and mGluR5) reduces behavioral effects of drugs o

93 of group I metabotropic glutamate receptors (mGluR1 and mGluR5).

94 opic glutamate receptors (mGluRs), including mGluR1 and mGluR5, are G protein-coupled receptors (GPCR

95 opic glutamate receptors (mGluRs), including mGluR1 and mGluR5, elicits translation-dependent neural

96 e in the ligand-dependent internalization of mGluR1 and mGluR5, members of the group I mGluR family.

97 he group I metabotropic glutamate receptors, mGluR1 and mGluR5, occurs through G-protein coupling, bu

98 I metabotropic glutamate receptors (mGluRs), mGluR1 and mGluR5, play critical functions in forms of a

99 I metabotropic glutamate receptors (mGluRs), mGluR1 and mGluR5, regulate activity in the globus palli

100 In neurons expressing mGluR1 and mGluR5, the selective NAMs each strongly inhi

101 gical evidence indicated involvement of both mGluR1 and mGluR5, which was further supported for mGluR

102 FC, repeated cocaine up-regulated Homer2a/b, mGluR1 and NR2b expression, without affecting Homer1b/c

103 The effects of co-infusing mGluR1 and PLC inhibitors were additive, whereas those o

104 Rdelta2 changes subcellular fractionation of mGluR1 and TRPC3 to increase their surface expression.

105 ctivator (i.e., endogenous biased agonism at mGluR1) and changes in spinal dynorphin/KOR signaling re

106 family C, metabotropic glutamate receptor 1 (mGluR1) and mGluR5.

107 diated by metabotropic glutamate receptor 1 (mGluR1) and NMDA receptors.

108 on group 1 metabotropic glutamate receptor (mGluR1) and PKC signaling, in contrast to an alternate L

109 the type I metabotropic glutamate receptor (mGluR1), and we found increased mGluR1 mRNA and protein

110 Finally, we show that ERalpha, ERbeta, mGluR1, and ERK all reside within specialized membrane m

111 rkers of MSN neurogenesis (Islet1, DARPP-32, mGluR1, and NeuN).

112 etermining residues in the group I receptor, mGluR1, and the group III receptors, mGluR4 and mGluR7.

113 tive G protein-coupled receptors, mGluR4 and mGluR1, and the taste bud-expressed heterodimer T1R1+T1R

114 Taken together, these results suggest that mGluR1 antagonism inhibits de novo protein synthesis; th

115 unit 1 (mGluR1) antagonism but not selective mGluR1 antagonism prevented neuronal injury.

116 -/metabotropic glutamate receptor subunit 1 (mGluR1) antagonism but not selective mGluR1 antagonism p

117 ROS scavengers (PBN, tempol), but not by an mGluR1 antagonist (LY367385) or NO synthase inhibitor (l

118 potentials after SNL, which was prevented by mGluR1 antagonist AIDA [(RS)-1-aminoindan-1,5-dicarboxyl

119 Furthermore, intra-VTA microinjections of mGluR1 antagonist JNJ16259685 and protein synthesis inhi

120 tral cells) was completely eliminated by the mGluR1 antagonist LY367385 [(S)-(+)-alpha-amino-4-carbox

121 After prolonged withdrawal, mice in which an mGluR1 antagonist was administered following cocaine sel

122 atodendritic DA release, whereas CPCCOEt, an mGluR1 antagonist, suppressed it.

123 on following acute injections of a selective mGluR1 antagonist.

124 llowing induction were reversibly blocked by mGluR1 antagonists [(S)-+-alpha-amino-4-carboxy-2-methyl

125 dependent component of LTD, normalization by mGluR1 antagonists requires the activation of protein sy

126 e discovery of a novel series of tetracyclic mGluR1 antagonists, such as 23c and 23e, with oral effic

127 bodies are similar to those of patients with mGluR1 antibodies.

128 , and Ma2), glutamic acid decarboxylase, and mGluR1 antibodies.

129 Antagonists of mGlur1 are suggested to be useful for the treatment of p

130 al validity, the present study also suggests mGluR1 as potential target for the treatment of autism s

131 ons of critical residues in the motif reduce mGluR1 association with lipid rafts and agonist-induced,

132 provide exciting new momentum for developing mGluR1-based pharmacology to treat ataxia.

133 However, a common mGluR1-based therapeutic strategy may be helpful for rec

134 LC were not, indicating that the efficacy of mGluR1 blockade to lower binge intake involves a pathway

135 Release suppression by mGluR1 blockade was prevented by 2-APB or CPA, indicatin

136 Activation of mGluR1 by the agonist 3,4-dihydroxyphenylglycol increase

137 the metabotropic glutamate receptor type 1 (mGluR1), by two entirely different methods: (i) UV light

138 ssing these receptors, combining a selective mGluR1 competitive antagonist with either an mGluR1- or

139 essing mGluR1 and mGluR2, combining the same mGluR1 competitive inhibitor with an mGluR1 or mGluR2 NA

140 -negative Galpha(i/o) proteins revealed that mGluR1 couples strongly to TRPC4beta through Galpha(i/o)

141 tors (MPEP), cocaine no longer decreased the mGluR1 current.

142 odulator JNJ16259685 shortened the prolonged mGluR1 currents and rescued the moderate ataxia.

143 ncing of the metabotropic glutamate receptor mGluR1 decreased Ca(2)(+) influx in PCs and reversed the

144 Both BBB-NiP and BBB-mGluR1 demonstrated a similar 20-fold enhanced rate of t

145 Type 1 metabotropic glutamate receptor (mGluR1)-dependent signaling at parallel fiber to Purkinj

146 We further show that caveolin-1 attenuates mGluR1-dependent activation of extracellular signal-regu

147 iation with lipid rafts and agonist-induced, mGluR1-dependent activation of extracellular-signal-acti

148 d activation of distinct sources of Ca2+ and mGluR1-dependent facilitation of NMDAR function.

149 ated translation machinery in the VTA via an mGluR1-dependent mechanism.

150 estrogen receptor to stimulate postsynaptic mGluR1-dependent mobilization of the endocannabinoid ana

151 otential 3 (TRPC3), which is also needed for mGluR1-dependent slow EPSCs and motor coordination and a

152 , 12 weeks) we find prolonged parallel fiber mGluR1-dependent synaptic currents and calcium signaling

153 ss of GluRdelta2 disrupts the time course of mGluR1-dependent synaptic transmission at parallel fiber

154 naptic transmission from mGluR5-dependent to mGluR1-dependent.

155 Differential signaling by mGluR1, depending on its activation by membrane estrogen

156 s the occupancy of both binding sites in the mGluR1 dimer.

157 RET response reports active conformations of mGluR1 dimers.

158 Downstream of mGluR1, dysregulation of calcium homeostasis has been hy

159 ng mutation of F585I/mGluR5 in mGluR1 (F599I/mGluR1) eliminates CPPHA's effect without altering the p

160 regions of tamalin played critical roles in mGluR1 endocytosis.

161 ue to central target-mediated removal of the mGluR1-engaging antibody.

162 normal resting levels while in wildtype PNs mGluR1 EPSCs are enhanced by elevated [Ca(2+)].

163 Fitting with this, mGluR1-evoked inward currents are increased in GluRdelta

164 both induced rapid bilateral upregulation of mGluR1 expression in cytoplasmic and synaptic fractions

165 he corresponding mutation of F585I/mGluR5 in mGluR1 (F599I/mGluR1) eliminates CPPHA's effect without

166 In SCA2 PNs, enhanced mGluR1 function is prevented by buffering [Ca(2+)] at no

167 Studies of mGluR1 function showed increased hippocampal mGluR1-indu

168 elevated intracellular calcium and enhanced mGluR1 function, a mechanism likely to contribute to PN

169 Metabotropic glutamate receptor 1 (mGluR1) function in Purkinje neurons (PNs) is essential

170 hesis that mGluR5 coordinates a reduction in mGluR1 functional activity after cocaine treatment.

171 cond goal was to use the relative density of mGluR1 gene transcripts in brain regions to estimate spe

172 g kg(-1) per 2 h(-1)) elevated CeA levels of mGluR1, GluN2B, Homer2a/b and phospholipase C (PLC) beta

173 s and motor coordination and associates with mGluR1, GluRdelta2, and PKCgamma.

174 n require metabotropic glutamate receptor 1 (mGluR1, Grm1).

175 However, blocking mGluR1 had no effect on the firing activity of PVN neuro

176 viously identified allosteric potentiator of mGluR1 has the opposite effect.

177 s across an in vitro BBB model compared with mGluR1 IgG fused to a control antibody fragment.

178 NL was followed by bilateral upregulation of mGluR1 in 5-HT(2A)R-containing postsynaptic densities.

179 be suggested by observed expression of GRM1/mGluR1 in a number of RCC tumor biopsy samples and cell

180 ic approach to identify protein partners for mGluR1 in cerebellum and discovered glutamate receptor d

181 ther, these data reveal higher expression of mGluR1 in DA neurons, suggesting potential differences i

182 f cocaine decreased the current activated by mGluR1 in dopamine neurons, and it had no effect on the

183 luated the ability of (18)F-FIMX to quantify mGluR1 in humans.

184 be an effective PET radioligand for imaging mGluR1 in monkey brain and therefore merits further eval

185 Upregulation of mGluR1 in synaptic compartments was partially prevented

186 Because of the pivotal role of mGluR1 in the control of cocaine-induced plasticity, we

187 In addition, protein levels of mGluR1 in the enriched synaptosomal fraction from both t

188 uced plasticity, we investigated the role of mGluR1 in the formation of drug cue-mediated cocaine see

189 (18)F-FIMX can quantify mGluR1 in the human brain with a 120- to 170-min scan.

190 antifying metabotropic glutamate receptor 1 (mGluR1) in monkey brain.

191 ssed metabotropic glutamate receptor 1 (Grm1/mGluR1) in mouse models of melanoma.

192 uman brain metabotropic subtype 1 receptors (mGluR1) in neuropsychiatric disorders and in drug develo

193 ynaptic changes during maintenance of cL-LTP(mGluR1) in rat hippocampus.

194 the group I metabotropic glutamate receptor mGluR1 increases the strength of this efferent inhibitio

195 ete perceptual units for processing, whereas mGluR1-induced alpha may serve the purpose of blocking u

196 In our model of mGluR1-induced alpha, TC cells are equally likely to fir

197 mGluR1 function showed increased hippocampal mGluR1-induced long-term depression in the adult offspri

198 s can be modulated and may contribute to the mGluR1-induced plasticity changes in Purkinje cells.

199 Furthermore, we found that tamalin regulates mGluR1 internalization by interacting with S-SCAM, a pro

200 We also show here that the mGluR1 internalization is dependent on a specific E3 ubi

201 caveolin-1 controls the rate of constitutive mGluR1 internalization, thereby regulating expression of

202 precipitation showed that ERalpha-mGluR1 and mGluR1-IP3R complexes exist in both sexes but are regula

203 The metabotropic glutamate receptor 1 (mGluR1) is a Galpha(q)-protein-coupled receptor and is d

204 The metabotropic glutamate receptor 1 (mGluR1) is abundantly expressed in the mammalian central

205 n Eif4ebp2(-/-) mice by using antagonists of mGluR1 (JNJ16259685) or mGluR5 (fenobam).

206 that is abolished in cells expressing mutant mGluR1 lacking intact caveolin binding motifs.

207 Thus, both mGluR1-linked IP(3)R- and RyR-dependent ER Ca(2+) stores

208 yphenylglycine in combination with either an mGluR1 (LY367385) or an mGluR5 (3-[(2-methyl-4-thiazolyl

209 ent receptor activities, primarily involving mGluR1, maintain excitatory cellular responses and emerg

210 analysis of synaptic responses during cL-LTP(mGluR1) maintenance revealed an increased number of quan

211 mation flow through the AOB and suggest that mGluR1 may be an important locus for experience-dependen

212 Furthermore, they suggest that activation of mGluR1 may represent a potential strategy for reducing c

213 ed a metabotropic glutamate receptor type 1 (mGluR1)-mediated late long-term potentiation (LTP) of ex

214 n (DSE) and metabotropic glutamate receptor (mGluR1)-mediated synaptic depression are mediated by 2-A

215 Through metabotropic glutamate receptor 1 (mGluR1)-mediated synaptic depression, mGluR1 positive al

216 and PACAP treatment reversed the decrease in mGluR1-mediated calcium current modulation associated wi

217 ired for the cocaine-mediated suppression of mGluR1-mediated currents in dopamine neurons.

218 At parallel fiber synapses, mGluR1-mediated excitatory postsynaptic currents (EPSCs)

219 bition of protein translation eliminated the mGluR1-mediated inhibition and restored the mGluR5 respo

220 sed mGluR1-mediated responses, and deficient mGluR1-mediated long-term potentiation.

221 d by the PF-associated Ca(2+) influx via the mGluR1-mediated nonselective cation conductance.

222 e antibody with thalamic neurons involved in mGluR1-mediated pain processing.

223 -29), selectively potentiates mGluR5 but not mGluR1-mediated responses in midbrain neurons, whereas a

224 at Purkinje cell dendritic spines, decreased mGluR1-mediated responses, and deficient mGluR1-mediated

225 Likewise, mGluR1-mediated synaptic depression, induced either by h

226 An intra-CeA infusion of mGluR1, mGluR5 and PLC inhibitors all dose-dependently r

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

228 Western blots revealed that levels of mGluR1, mGluR5, or cannabinoid receptor (CB1R) were unch

229 Finally, evidence for a similar mGluR1/mGluR5 functional dependence is shown in medium s

230 substantive evidence that the inhibition of mGluR1/mGluR5 is an effective treatment for physiologica

231 posure did not alter D1 receptor function or mGluR1 modulation of firing.

232 mGluR1 modulation of intrinsic conductances is otherwise

233 te receptor (mGluR1), and we found increased mGluR1 mRNA and protein in hippocampus from the adult of

234 re, Group I metabotropic glutamate receptor (mGluR1) mRNA levels were altered in several brain region

235 to the potency of L-glutamate activation in mGluR1 mutants and others that diminished the potency/ef

236 In mGluR1, mutation of the corresponding residue, V909, to

237 f the potent and specific activity-dependent mGluR1-negative allosteric modulator JNJ16259685 shorten

238 AR protein levels after OGD was prevented by mGluR1 or A(3) receptor antagonists, indicating that AMP

239 he same mGluR1 competitive inhibitor with an mGluR1 or mGluR2 NAM yielded partial and full inhibition

240 Whereas L-SOP cannot activate mGluR1 or mGluR2, it acts as a weak antagonist for mGluR

241 A receptor blocker) or by selective block of mGluR1 or mGluR2.

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

243 induced depolarization was reduced by either mGluR1 or mGluR5 antagonists, suggesting involvement of

244 uR-LTD) in Eif4ebp2(-/-) mice was rescued by mGluR1 or mGluR5 antagonists.

245 bryonic kidney 293) cells cotransfected with mGluR1 or mGluR5.

246 rrent (DISC) is attenuated by antagonists of mGluR1 or TRP channels.

247 vented by metabotropic glutamate receptor 1 (mGluR1) or A(3) receptor antagonists, indicating a role

248 mGluR1 competitive antagonist with either an mGluR1- or mGluR5-selective negative allosteric modulato

249 we found that systemic administration of an mGluR1 PAM attenuated the expression of incubated cravin

250 Together, these results indicate that mGluR1 plays a critical role in controlling information

251 n by administering repeated injections of an mGluR1 positive allosteric modulator (PAM) prevented CP-

252 phthyl acetyl spermine injection or systemic mGluR1 positive allosteric modulator administration.

253 ing test, or 3) systemic administration of a mGluR1 positive allosteric modulator followed by a seeki

254 tor 1 (mGluR1)-mediated synaptic depression, mGluR1 positive allosteric modulators remove CP-AMPARs f

255 Subtype 1 of the group I mGluR family (mGluR1) probably regulates a K+ channel, whereas mGluR5

256 ions, the initial intersubunit activation of mGluR1 proceeds with millisecond speed, that there is lo

257 ERalpha and ERbeta physically interact with mGluR1, providing a means through which ERs may activate

258 mitral cells, which was blocked by NMDA and mGluR1 receptor antagonists, converting mitral cell resp

259 The results highlight presynaptic roles of mGluR1 receptors and of BDNF as a retrograde signal to r

260 Here, we show that mGluR1 recruitment to lipid rafts is enhanced by agonist

261 glutamate receptors (mGluRs), and especially mGluR1, remains equivocal.

262 Among these, mGluR1 responds to L-glutamate effectively, whereas it b

263 sustained current component of the biphasic mGluR1 response.

264 vo Comparative assessment of BBB-NiP and BBB-mGluR1 revealed that, whereas their serum pharmacokineti

265 altering the potentiation of a known PAM of mGluR1, (S)-2-(4-fluorophenyl)-1-(toluene-4-sulfonyl)pyr

266 antagonist MCPG, and partially inhibited by mGluR1-selective allosteric modulators.

267 and PPD were eliminated by treatment with an mGluR1-selective antagonist.

268 ), cerebellum, and amygdala), stimulation of mGluR1 selectively inhibits synaptic transmission mediat

269 velopment and for motor learning and altered mGluR1 signaling causes ataxia.

270 Thus, GluRdelta2 is part of the mGluR1 signaling complex needed for cerebellar synaptic

271 activated metabotropic glutamate receptor 1 (mGluR1) signaling, are critical to the transition from a

272 ement is blocked by application of a group I mGluR1-specific antagonist, indicating that enhancement

273 ely suppresses inhibition in females through mGluR1 stimulation of phospholipase C, leading to inosit

274 phosphatase 2A (PP2A) is overactivated after mGluR1 stimulation, and tyrosine phosphatase is overacti

275 lation is almost exclusively mediated by the mGluR1 subtype.

276 tions, the initial rearrangement between the mGluR1 subunits occurs at a speed of tau (1) ~ 1-2 ms an

277 We found that decreased mGluR1 surface expression in the NAc preceded and enable

278 t confers CaM binding dramatically increases mGluR1 surface expression, whereas the analogous mutatio

279 Central mGluR1 target engagement after systemic administration w

280 Likewise, another mutation (V757L/mGluR1) that abolishes potentiation of Ro 67-7476 has no

281 us dominant mutations in GRM1, which encodes mGluR1, that are associated with distinct disease phenot

282 rrent produced by activation of postsynaptic mGluR1, thereby constituting a useful form of feedback r

283 of brain uptake with the relative density of mGluR1 transcript allows specific receptor binding of a

284 values in brain regions correlated well with mGluR1 transcript density, and the correlation suggested

285 ccumulation and incubation, whereas blocking mGluR1 transmission at even earlier withdrawal times acc

286 Thus, restoring mGluR1 transmission by administering repeated injections

287 tion and pain after nerve injury and support mGluR1 upregulation as a novel feedforward activation me

288 l], confirming 5-HT(2A)R-mediated control of mGluR1 upregulation triggered by SNL.

289 The mutation in mGluR1 (V909L) that confers CaM binding dramatically inc

290 olecules, metabotropic glutamate receptor-1 (mGluR1), voltage-gated sodium channels (Nav ) and glutam

291 Western blotting analysis indicates that mGluR1 was coupled to extracellular signal-regulated kin

292 5-HT(2A)R and mGluR1 were found to be coexpressed in postsynaptic dens

293 of DHPG in the cocaine group was mediated by mGluR1 whereas its effect in the saline group was mediat

294 Also, CREB knockdown impaired cL-LTP(mGluR1), whereas CREB overexpression facilitated the ind

295 in interaction between a synaptic kinase and mGluR1, which constitutes a feedback loop facilitating d

296 vity of the metabotropic glutamate receptor, mGluR1, which is known to couple with ERalpha at the pla

297 e, LTP requires inhibition of SK channels by mGluR1, which removes a negative feedback loop that cons

298 ed evoked potentials during costimulation of mGluR1 with 3,5-DHPG [(RS)-3,5-dihydroxyphenylglycine].

299 ake, reflecting the expected distribution of mGluR1 with notably high uptake in cerebellum, which bec

300 Therefore, activation of mGluR1 with positive allosteric modulators (PAM) may red