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 ain was bound specifically and reversibly to mGluR1.

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

5 n reported in association with antibodies to mGluR1.

6 c acetylcholine receptor, or via coexpressed mGluR1.

7 volved in the ligand-mediated endocytosis of 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 tinct from that of allosteric antagonists of mGluR1.

12 likely involves glutamate signaling through mGluR1.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

29 to identify distinct ion channel targets for mGluR1/5 receptors in striatal cholinergic interneurons:

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 data suggest that allosteric potentiators of mGluR1 act at a site that is distinct from that of allos

53 2-amino-2-(3,5-dihydroxyphenyl) acetic acid (mGluR1)-activated TPRC3 current as for recombinant TRPC3

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

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

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

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

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

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

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

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

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

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

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

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

66 mGluR1 alpha and TrkB immunoreactivities were invariably

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

88 of group I metabotropic glutamate receptor (mGluR1 and mGluR5) activation on identified melanin-conc

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

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

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

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

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

94 st, a combined activation of group I mGluRs (mGluR1 and mGluR5) induces a transient depression that i

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

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

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

98 up I metabotropic glutamate receptor family, mGluR1 and mGluR5, both couple to G(q) to mediate rises

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

100 DHPG, acting at mGluR1 and mGluR5, increased the rate but not amplitude

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

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

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

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

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

106 involves the metabotropic glutamate receptor mGluR1 and phospholipase-C (PLC).

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

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

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

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

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

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

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

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

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

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

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

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

119 ultures, an effect prevented by System x(c)-/mGluR1 antagonism.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

139 Here, two divergent mGluR1 Ca2+-signalling pathways and the associated membr

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

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

142 mGluR1 contribution was unexpected because its activatio

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

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

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

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

147 Additionally, cultures derived from mGluR1-deficient mice exhibited the same potentiation in

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

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

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

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

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

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

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

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

156 , 12 weeks) we find prolonged parallel fiber mGluR1-dependent synaptic currents and calcium signaling

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

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

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

160 RET response reports active conformations of mGluR1 dimers.

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

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

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

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

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

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

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

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

169 Studies of mGluR1 function showed increased hippocampal mGluR1-indu

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

187 Upregulation of mGluR1 in synaptic compartments was partially prevented

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

225 ses, in parallel with a facilitation of slow mGluR1 (metabotropic glutamate receptor type 1)-mediated

226 the metabotropic glutamate receptor subunits mGluR1, mGluR3, mGluR4, mGluR5, and mGluR7.

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

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

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

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

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

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

233 mGluR1 modulation of intrinsic conductances is otherwise

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

252 Metabotropic glutamate receptor 1 (mGluR1) plays important roles in the neurotransmission a

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

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

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

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

257 ced depolarization desensitized; blockade of mGluR1 prevented the desensitization.

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

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

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

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

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

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

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

265 sustained current component of the biphasic mGluR1 response.

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

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

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

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

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

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

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

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

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

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

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

277 lation is almost exclusively mediated by the mGluR1 subtype.

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

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

280 Central mGluR1 target engagement after systemic administration w

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

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

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

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

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

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

287 Thus, restoring mGluR1 transmission by administering repeated injections

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

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

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

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

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

293 5-HT(2A)R and mGluR1 were found to be coexpressed in postsynaptic dens

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

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

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

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