ライフサイエンスコーパス: mGluR2

1 n of metabotropic glutamate receptor type 2 (mGluR2).

2 metabotropic glutamate subtype 2 receptors (mGluR2).

3 R and the metabotropic glutamate receptor 2 (mGluR2).

4 that leads to largely uncompensated loss of mGluR2.

5 blocker) or by selective block of mGluR1 or mGluR2.

6 from R1a increased the surface stability of mGluR2.

7 n of specific receptor populations, such as, mGluR2.

8 olved heteromerization between 5-HT(2A)R and mGluR2.

9 t group I receptors and is a good agonist of mGluR2.

10 which allosteric drugs activate and modulate mGluR2.

11 h the reported intracerebral distribution of mGluR2.

12 a specific PET ligand for in vivo imaging of mGluR2.

13 y a mutation that disrupts the gene encoding mGluR2.

14 n of the otherwise plasma membrane-localized mGluR2.

15 erotonergic and glutamatergic drugs bind the mGluR2/2AR heterocomplex, which then balances Gi- and Gq

16 We find that the mGluR2/2AR-mediated changes in Gi and Gq activity predic

17 d group II/III mGluRs, including variants of mGluR2, 3, 6, 7, and 8.

18 r dopamine that was reversed by infusing the mGluR2/3 agonist (2R,4R)-4-aminopyrrolidine-2,4-dicarbox

19 ication of this reaction to the synthesis of mGluR2/3 agonist 1 (43% overall yield) and a few interme

20 R, as well as the HTR-blocking effect of the mGluR2/3 agonist and antipsychotic drug in development L

21 n with a maximum tolerated dose (MTD) of the mGluR2/3 agonist LY379268 (20mg/kg) beginning at 4 weeks

22 Our data thus suggest that mGluR2/3 agonist regulates postsynaptic AMPA receptors b

23 In vivo iontophoretic application of the mGluR2/3 agonists (2R, 4R)-APDC or LY379268 onto dlPFC D

24 mGluR2/3 agonists (2S,1'R,2'R'3'R)-2-(2,3-dicarboxycyclo

25 Although previous studies have shown that mGluR2/3 agonists have no effect on dopamine (DA) in wil

26 the synthesis of other bicyclo[3.1.0]hexane mGluR2/3 agonists is discussed.

27 anced neuronal firing following low doses of mGluR2/3 agonists.

28 Staining for mGluR2/3 also was seen in amacrine processes postsynapti

29 Positive immunoreactivity is found for mGluR2/3 and 5.

30 used two polyclonal antisera to mGluR1a and mGluR2/3 and confocal laser microscopy to investigate th

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

32 Immunoreactivity for mGluR2/3 and mGluR5 as observed in fibers and putative a

33 of metabotropic glutamate receptors (mGluRs) mGluR2/3 and mGluR5 in laminae I and II of the dorsal ho

34 g depends on the balance between stimulating mGluR2/3 and mGluR5 in the NAcore, and the efficacy of N

35 Electron microscopy showed that both mGluR2/3 and mGluR5 were in perikarya, dendrites, and ve

36 induce LTP and LTD by indirectly stimulating mGluR2/3 and mGluR5, respectively.

37 d from the high percentage of single-labeled mGluR2/3 and mGluR8 cells, there is a considerable popul

38 at increased glutamate activates presynaptic mGluR2/3 and mGluR8 receptors but not mGluR4, although t

39 ese results support further investigation of mGluR2/3 and other glutamate-targeted treatments for sch

40 Infusion of the mGluR2/3 antagonist (RS)-1-amino-5-phosphonoindan-1-carb

41 The mGluR2/3 antagonist LY341495 blocked these behavioral an

42 a demonstrate the potentiation effect of the mGluR2/3 antagonist LY341495 on DOI-induced HTR, as well

43 e mGluR2 agonist LY395756 and was blocked by mGluR2/3 antagonist LY341495.

44 The enhancing effects were reversed by an mGluR2/3 antagonist or by activating cAMP signaling, con

45 s effect was blocked by pretreatment with an mGluR2/3 antagonist.

46 In contrast, mGluR1alpha and mGluR2/3 are expressed by mainly small and medium cells.

47 patterns indicate that both mGluR1alpha and mGluR2/3 are positioned for postsynaptic function, where

48 Down-regulation of mGluR2/3 at the mossy fibers and the SLM may render epil

49 to be mediated by activation of presynaptic mGluR2/3 autoreceptors secondary to AM251-induced increa

50 ing, nor was potentiated reinstatement after mGluR2/3 blockade reduced by blocking nNOS.

51 reinstated sucrose seeking in the absence of mGluR2/3 blockade was not affected by blocking mGluR5.

52 Potentiated sucrose reinstatement by mGluR2/3 blockade was reversed by antagonizing mGluR5, b

53 rose reinstatement was potentiated following mGluR2/3 blockade.

54 In both regions, mGluR2/3 caused a long-lasting reduction of glutamate re

55 stry showed that the laminar distribution of mGluR2/3 changed with the critical period and was sensit

56 nt plasticity by studying the correlation of mGluR2/3 changes with the critical period of ocular domi

57 ocortical afferent segregation indicate that mGluR2/3 circuitry in the visual cortex is influenced by

58 The localization of mGluR2/3 differed regionally, with postsynaptic labeling

59 Stimulation of mGluR2/3 evoked a direct, TTX-insensitive membrane hyper

60 a marked and progressive down-regulation of mGluR2/3 expression in mossy fiber at hilus and CA3 stra

61 Here, we explore whether mGluR2/3 expression is affected in a rat model of tempor

62 therapeutics based on rodent research, where mGluR2/3 have been shown to reduce axonal glutamate rele

63 amate can modulate dopamine transmission via mGluR2/3 heteroreceptors.

64 A dramatic lessening of mGluR2/3 immunofluorescence was observed at CA1 and CA3

65 presynaptic axon terminals were labeled for mGluR2/3 immunoreactivity and formed asymmetrical synaps

66 mGluR2/3 immunoreactivity was mainly localized in astroc

67 The mGluR2/3 immunostaining became most intense in layer IV

68 mGluR2/3 immunostaining was distributed only in the neur

69 ating evidence suggests the critical role of mGluR2/3 in different aspects of nicotine addiction, inc

70 The involvement of mGluR2/3 in other neuropsychiatric conditions, such as a

71 examine structure-function relationships for mGluR2/3 in the basolateral amygdala (BLA) and bed nucle

72 glutamate receptors 1alpha (mGluR1alpha) and mGluR2/3 in the cat retina was studied through the use o

73 and exploring the effects of dark rearing on mGluR2/3 in the primary visual cortex of cats.

74 oelectron microscopy identified postsynaptic mGluR2/3 in the spines, in addition to the traditional p

75 y activating cAMP signaling, consistent with mGluR2/3 inhibiting postsynaptic cAMP signaling in spine

76 In the molecular layer, mGluR2/3 labeling slightly declined in the 1-month post-

77 of dark rearing and the correlation of early mGluR2/3 laminar changes with geniculocortical afferent

78 The current study examined mGluR2/3 localization and actions in the primate dlPFC l

79 provides convincing evidence suggesting that mGluR2/3 may provide an effective therapeutic approach f

80 mixed results in patients, and understanding mGluR2/3 mechanisms in primates will help guide therapeu

81 is with Ca(2+) chelators largely blocked the mGluR2/3 modulation of NMDAR currents.

82 Our data support the presence of mGluR2/3 on the terminals of corticostriatal afferents,

83 p I mGluR1alpha also express either group II mGluR2/3 or group III mGluR8.

84 In the second experiment, blocking mGluR2/3 prevented the ability of N-acetylcystine to inh

85 dies, dendrites, and axonal fibers and light mGluR2/3 processes.

86 This focused review article highlights that mGluR2/3 provide a promising target in the search for sm

87 or weeks and elevated the normally declining mGluR2/3 quantity shortly after the peak of the critical

88 stead involve the anti-excitotoxic action of mGluR2/3 receptor agonists.

89 post-synaptic receptors (AMPA, NMDA, GABA-A, mGluR2/3 receptors and Nav, Cav voltage-gated ion channe

90 Blockade of NAc metabotropic glutamate mGluR2/3 receptors by LY341495 [(2S)-2-amino-2-[(1S,2S)-

91 l, our observations suggest that mGluR1a and mGluR2/3 receptors have distinct cellular localizations

92 Our results demonstrate a complex role for mGluR2/3 receptors in modulating anxiety circuitry, incl

93 vation of either presynaptic D1 receptors or mGluR2/3 receptors may critically regulate the direction

94 These findings suggest that activation of mGluR2/3 receptors potentiates NMDAR channel functions i

95 Significantly, blockade of either D1 or mGluR2/3 receptors unmasked 10 Hz stimulation-induced LT

96 NMDAR currents, suggesting the mediation by mGluR2/3 receptors.

97 ion was developmentally regulated, with only mGluR2/3 showing expression at the embryonic day 19 deve

98 data indicate that dysregulated presynaptic mGluR2/3 signaling is a possible site of shared signalin

99 l stimulation of ERalpha or ERbeta triggered mGluR2/3 signaling, decreasing L-type calcium channel-me

100 Our data suggest that low doses of mGluR2/3 stimulation may have therapeutic effects throug

101 Our data suggest that mGluR2/3 together with another sensory-influenced mGluR,

102 Expression of mGluR2/3 was clearly evident in cell bodies, dendrites,

103 xc- to regulate excitatory transmission via mGluR2/3 was determined.

104 mGluR2/3 was mainly in the inner part of lamina II; mGlu

105 Immunostaining for mGluR2/3 was observed in horizontal cells as well as in

106 The group 2 metabotropic glutamate receptor (mGluR2/3) agonist, pomaglumetad methionil (POM), showed

107 Two metabotropic glutamate receptor 2/3 (mGluR2/3) agonists (pomaglumetad [POMA] and TS-134) were

108 of the metabotropic glutamate receptors 2/3 (mGluR2/3) and 5 (mGluR5).

109 c group II metabotropic glutamate receptors (mGluR2/3) and thereby inhibiting excitatory transmission

110 ry metabotropic glutamate receptors 2 and 3 (mGluR2/3) are key autoreceptors on glutamatergic termina

111 ologically, whereas Group II mGluR proteins (mGluR2/3) are mainly associated with neuroglia.

112 receptor subtypes (mGluR1alpha, mGluR5, and mGluR2/3) during postnatal development of mouse ventral

113 l functions of postsynaptic group II mGluRs (mGluR2/3) in PFC neurones, we investigated the molecular

114 mined the involvement of cAMP-linked mGluRs (mGluR2/3) in sensory-dependent plasticity by studying th

115 f group II metabotropic glutamate receptors (mGluR2/3) in the amygdala plays a critical role in the r

116 oup I (mGluR1alpha and mGluR5) and group II (mGluR2/3) metabotropic glutamate receptor subtypes were

117 n of D1 and group II metabotropic glutamate (mGluR2/3) receptors act to nullify any net change in syn

118 y group II metabotropic glutamate receptors (mGluR2/3) via a cAMP-dependent protein kinase mechanism.

119 Group II metabotropic glutamate receptors (mGluR2/3), which couple to Gi/Go, have been a focus of t

120 etabotropic glutamate receptors mGluR1alpha, mGluR2/3, and mGluR5; and the intracellular signaling mo

121 ility is negatively regulated by presynaptic mGluR2/3, and sucrose reinstatement was potentiated foll

122 polar brush cells are immunoreactive to anti-mGluR2/3, anticalretinin, and anticalbindin.

123 followed by group II, with 51.6% expressing mGluR2/3, followed by group I, with only 6.8% expressing

124 Both UBC subsets were mGluR2/3, GluR2/3, and NMDAR1 immunoreactive.

125 amate receptor subunits GluR2/3, NMDAR1, and mGluR2/3, like they do in the mature mouse cerebellum in

126 In contrast, mGluR1 alpha, mGluR2/3, mGluR4a, and mGluR7 were expressed in leptomen

127 mGluR2/3, mGluR4a, mGluR5, and mGluR7 were also expresse

128 re strongly immunoreactive for mGluR1 alpha, mGluR2/3, mGluR4a, mGluR5, and mGluR7.

129 , delta 1/2) and metabotropic (mGluR1 alpha, mGluR2/3, mGluR5) glutamate receptor subtypes.

130 expression of four types of mGluRs: mGluRla, mGluR2/3, mGluR5, and mGluR7 in the dorsal and ventral a

131 Immunopositivity for mGluRs, especially mGluR2/3, was present in vesicle-containing profiles app

132 tergic synaptic currents in the NAcore in an mGluR2/3-dependent manner, while high doses of NAC incre

133 ptors caused a time-dependent attenuation of mGluR2/3-induced depotentiation of previously induced LT

134 Neither mGluR1a-ir nor mGluR2/3-ir could be detected in TH-ir soma within subst

135 e puncta were abundant; unlike mGluR1a, many mGluR2/3-ir puncta colocalized with SV2-ir, and striatal

136 puncta colocalized with SV2-ir, and striatal mGluR2/3-ir puncta were markedly reduced in number after

137 luR1a-ir staining, similar punctate neuropil mGluR2/3-ir staining was observed within all basal gangl

138 by the metabotropic glutamate receptor 2/3 (mGluR2/3-LTD) remains intact.

139 Additionally, thickness of mGluR2/3-stained SLM layer narrowed up to 70% of control

140 ssary for ER alpha and ER beta activation of mGluR2/3.

141 om activation of either pre- or postsynaptic mGluR2/3.

142 EPSCs was reversed by blocking either xc- or mGluR2/3.

143 antiporter is a source of endogenous tone on mGluR2/3.

144 eceptors (mGluRs) or orthosteric agonists of mGluR2/3.

145 botropic glutamate receptors mGluR1alpha and mGluR2/3; the intracellular signaling molecules calcineu

146 In SCG neurons, mGluR2/4 dimers were not inhibited by the mGluR2-selecti

147 Under conditions that favor mGluR2/4 heterodimer formation, activation of the recept

148 Here, this question was addressed for the mGluR2/4 heterodimer, examined by coexpressing both rece

149 responses through mGluR2/4, suggesting that mGluR2/4 heterodimers are not modulatable by PAMs that a

150 ed to potentiate glutamate responses through mGluR2/4, suggesting that mGluR2/4 heterodimers are not

151 Strikingly, the mGluR2/7 heterodimer has high affinity and efficacy.

152 nformational pathway to activation, in which mGluR2/7 partially activates in the Apo state, even when

153 mGluR2/7 shows cooperativity in which an unliganded subu

154 unusually broad dynamic range should enable mGluR2/7 to respond to both glutamate transients from ne

155 ndogenous metabotropic glutamate receptor 2 (mGluR2), a Family C GPCR, in primary cortical neurons.

156 Alignment between mGluR3 and mGluR2, a closely related group II receptor, indicated t

157 for such well characterized GPCR dimers like mGluR2, a single 7TM is sufficient for G-protein couplin

158 d by hallucinogenic drugs, and activation of mGluR2 abolishes hallucinogen-specific signalling and be

159 While phase inversion is produced by an mGluR2-activated outward conductance in OFF-UBCs, the ph

160 ctive Galphai2-expressing mice suggests that mGluR2 activation may serve as a metaplastic switch to p

161 d that membrane hyperpolarization, either by mGluR2 activation of potassium channels, or by somatic c

162 This effect was mimicked by the selective mGluR2 agonist LY395756 and was blocked by mGluR2/3 anta

163 SAR218645 potentiated mGluR2 agonist-induced contralateral turning.

164 ase in vivo using nicotinic modulators or an mGluR2 agonist.

165 ]20f binds specifically and reversibly to an mGluR2 allosteric site, strongly suggesting that it is a

166 h encodes metabotropic glutamate receptor 2 (mGluR2), alters alcohol preference in animal models.

167 aneous viral delivery of the inhibitory SNAG-mGluR2 and excitatory light-activated ionotropic glutama

168 s prepared from a cell line expressing human mGluR2 and in primate brain slices.

169 ctive positive allosteric modulator at human mGluR2 and is without activity at human mGluR3.

170 hese results indicate distinct functions for mGluR2 and mGluR3 and suggest a dynamic regulation of mG

171 he group II metabotropic glutamate receptors mGluR2 and mGluR3 in the pathophysiology of schizophreni

172 t study was to distinguish the expression of mGluR2 and mGluR3 receptor proteins in schizophrenia and

173 tudy we aimed to determine how activation of mGluR2 and mGluR3 receptors (Group II) might modulate vi

174 Presynaptic group II metabotropic receptors (mGluR2 and mGluR3) are among different mechanisms that m

175 Group II metabotropic glutamate receptors (mGluR2 and mGluR3) may control relapse of alcohol seekin

176 , group II metabotropic glutamate receptors (mGluR2 and mGluR3) were suggested as targets for addicti

177 clic-AMP in RGT cells transfected with human mGluR2 and mGluR3.

178 clic-AMP in RGT cells transfected with human mGluR2 and mGluR3.

179 agonists were unable to discriminate between mGluR2 and mGluR3.

180 y significant effect on cells expressing the mGluR2 and mGluR4a receptors.

181 ntly, both positive allosteric modulators of mGluR2 and negative allosteric modulators of mGluR5 hold

182 s in mRNA levels of GAD(67), GAD(65), GAT-1, mGluR2, and neuronal nitric oxide synthase.

183 in cultured hippocampal neurons; mGluR1a and mGluR2 are targeted to dendrites and excluded from axons

184 (PAM) of metabotropic glutamate receptor 2 (mGluR2) are a potential therapy for anxiety, schizophren

185 Together, these data point to mGluR2 as an origin of alcohol preference and a potentia

186 ems, increasing the affinity of glutamate at mGluR2 as inferred by competition and GTPgamma(35)S bind

187 dies reveal that PKA directly phosphorylates mGluR2 at a single serine residue (Ser(843)) on the C-te

188 otion that positive allosteric modulators of mGluR2 block relapse-like behavior across different drug

189 These findings indicate that mGluR2 (but not mGluR3) can selectively modulate GABAerg

190 y contrast, in cells coexpressing mGluR1 and mGluR2, combining the same mGluR1 competitive inhibitor

191 ese regulatory changes indicate that the 2AR-mGluR2 complex may be involved in the altered cortical p

192 The 2AR-mGluR2 complex triggers unique cellular responses when t

193 are unable to form the interclass 5-HT(2A)R-mGluR2 complex, we demonstrated that heteromerization wa

194 loying this method, it was demonstrated that mGluR2 coupled strongly with Galphaob, Galphai1, Galphai

195 Previous work demonstrated that mGluR2 couples to pertussis toxin (PTX)-sensitive G prot

196 However, the specificity of mGluR2 coupling to individual members of the G(i/o) fami

197 h clozapine, but not with M100907, decreased mGluR2 density through a mechanism that involved heterom

198 In addition, mGluR2 did not seem to couple to the most divergent memb

199 Agonists for either 5-HT(2A)R or mGluR2 differentially affected trafficking through Rab5-

200 SNAG-mGluR2 enabled animals to discriminate parallel from per

201 Pharmacologic blockade of mGluR2 escalated alcohol self-administration in Wistar r

202 rd1 mice, photoswitch-charged mGluR2 ("SNAG-mGluR2") evoked robust OFF responses to light, but not i

203 d response to glutamate in a rat recombinant mGluR2 forced-coupled Ca(2+) mobilization assay.

204 horylation of this site inhibits coupling of mGluR2 from GTP-binding proteins

205 We first assessed modulation of mGluR2 function by AZD8529 using functional in vitro ass

206 enesis combined with biochemical measures of mGluR2 function reveal that phosphorylation of this site

207 c-prone state leads to specific reduction in mGluR2 function within the amygdala network and facilita

208 the precise mechanism by which PKA inhibits mGluR2 function.

209 om the superior cervical ganglion (SCG), the mGluR2/G protein coupling profile was characterized by r

210 mGluR2 (group II)-mediated inhibition of N-channels was

211 neurotransmission through activation of the mGluR2 has emerged as a new approach to treat schizophre

212 s expressing each component of the 5-HT(2A)R-mGluR2 heterocomplex alone, or together.

213 to one or both subunits of covalently linked mGluR2 homodimers reveals that receptor activation is hi

214 The causal role of mGluR2 in altered alcohol preference was further support

215 ndings provide evidence for a causal role of mGluR2 in cue-induced relapse to alcohol seeking.

216 1)C]13 is a potential PET imaging ligand for mGluR2 in different central nervous system-related condi

217 is sufficient to account for the actions of mGluR2 in each.

218 also augmented intracellular localization of mGluR2 in mouse frontal cortex pyramidal neurons.

219 fficacy of positive allosteric modulators of mGluR2 in nonhuman primate models of nicotine reinforcem

220 Using heterologously expressed mGluR2 in rat sympathetic neurons from the superior cerv

221 The compound behaves as a selective PAM of mGluR2 in recombinant and native receptor expression sys

222 mission tomography (PET) imaging ligands for mGluR2 in the brain.

223 is a promising candidate for PET imaging of mGluR2 in the brain.

224 odimerizes, and we find it to associate with mGluR2 in the hippocampus.

225 vivo in mice, where photoactivation of SNAP-mGluR2 in the medial prefrontal cortex reversibly modula

226 29 potentiated agonist-induced activation of mGluR2 in the membrane-binding assay and in primate cort

227 ic modulators (PAMs) of the mGlu receptor 2 (mGluR2) in a [(3)(5)S]GTPgammaS binding assay and were a

228 s of metabotropic glutamate type 2 receptor (mGluR2) in the BLA.

229 artments, and coexpression of 5-HT(2A)R with mGluR2 increased the intracellular distribution of the o

230 We also found that the activation of mGluR2 increases the phosphorylation of tau and that the

231 asmic tail, but not the equivalent region of mGluR2, inhibited PP2C assayed by using [32P]casein as a

232 r features such as inverted input signals or mGluR2 inhibition of Golgi cells.

233 ked GPCR, metabotropic glutamate 2 receptor (mGluR2), integrates ligand input, modulating signaling o

234 Here we show that the mGluR2 interacts through specific transmembrane helix do

235 nic subjects, the 2AR is upregulated and the mGluR2 is downregulated, a pattern that could predispose

236 rrant signaling, we subsequently showed that mGluR2 is increased in pyramidal neurons in the hippocam

237 Metabotropic glutamate receptor 2 (mGluR2) is a class 3 G protein-coupled receptor and an i

238 Whereas L-SOP cannot activate mGluR1 or mGluR2, it acts as a weak antagonist for mGluR1 and a po

239 studies were performed in recently available mGluR2 knockout and wildtype rats and in a monkey using

240 ography binding experiments in Wistar and in mGluR2 knockout and wildtype rats as well as in vivo bio

241 nd brain PET imaging studies in wildtype and mGluR2 knockout rats in a primate and in humans were per

242 ulture models to show that the activation of mGluR2 leads to the activation of extracellular signal-r

243 It is unknown how changed synaptic mGluR2 levels after adolescent nicotine exposure affect

244 m increase and lasting reduction in synaptic mGluR2 levels in the rat mPFC, causing attention deficit

245 together our findings strongly suggest that mGluR2 may participate in mediating the survival of neur

246 Furthermore, mGluR2-mediated dendritic compartmentalization in SACs i

247 SAR218645 augmented the mGluR2-mediated response to glutamate in a rat recombina

248 has a similar inhibitory effect on putative mGluR2-mediated responses at the medial perforant path s

249 Expression of mGluR2 metabotropic glutamate receptors, another pertuss

250 Unlike mGluR2, mGluR3 displays basal dynamics, which are Ca(2+)

251 The normal expression levels of mGluR2, mGluR3, and GCP II were determined for 10 region

252 ls in the type 1 metabotropic GluR (mGluR1), mGluR2, mGluR3, but not the mGluR5 subtype of G protein-

253 demonstrated the antipsychotic efficacy of a mGluR2/mGluR3 agonist.

254 luR3 receptor in the antipsychotic action of mGluR2/mGluR3 agonists.

255 ikingly, this cooperativity is asymmetric in mGluR2/mGluR3 heterodimers.

256 nd in zebrafish in vivo, where we found that mGluR2 modulated the threshold for escape behavior.

257 we use AZD8529, a novel positive allosteric mGluR2 modulator, to determine the role of this receptor

258 epticus induced a reduction in expression of mGluR2 mRNA in granule cells of the dentate gyrus.

259 luR1 competitive inhibitor with an mGluR1 or mGluR2 NAM yielded partial and full inhibition of the re

260 a selective positive allosteric modulator of mGluR2, on abuse-related effects of nicotine in squirrel

261 ddition of the mGluR7 C-terminal sequence to mGluR2 or to the unrelated somatodendritic protein telen

262 s metabotropic glutamate receptors, mGluR1a, mGluR2, or mGluR8.

263 Treating panic-prone rats with mGluR2 PAM blocked sodium lactate (NaLac)-induced panic

264 nd in a monkey using a structurally distinct mGluR2 PAM ligand with affinity for the same site, demon

265 site of mGluR2, was evaluated as a selective mGluR2 PAM PET tracer.

266 S binding assay and were able to displace an mGluR2 PAM radioligand, which we had previously develope

267 of patients with comorbid PD, treatment with mGluR2 PAM resulted in complete remission of panic sympt

268 e amygdala network and facilitates fear, and mGluR2 PAMs could be a targeted treatment for panic symp

269 mGluR2 participates in at least three types of mossy fib

270 de from pathophysiologic imaging studies, an mGluR2 PET tracer would enable confirmation of sufficien

271 se studies describe a potent brain penetrant mGluR2 positive allosteric modulator (PAM), SAR218645.

272 s-induced alcohol seeking was blocked by the mGluR2 positive allosteric modulator.

273 Application of an mGluR2-positive allosteric modulator (PAM) reduced gluta

274 ontal cortex in schizophrenia subjects, with mGluR2 protein levels unchanged.

275 mGluR2 receptor expression was absent, synaptic glutamat

276 Thus mGluR2 receptors could have a function in activity-depen

277 n of tau and that the specific activation of mGluR2 reduces oxidative stress mediated cytotoxicity in

278 of LY487379 potentiated synaptically evoked mGluR2 responses.

279 Thus, SNAG-mGluR2 restores patterned vision and combinatorial light

280 monstrated that [(11)C]13 accumulated in the mGluR2-rich brain regions.

281 combined application of mGluR4 PAMs with the mGluR2 selective PAM biphenyl indanone-A failed to poten

282 ion of the receptor was not evident with the mGluR2-selective agonist (2S,2'R,3'R)-2-(2',3'-dicarboxy

283 s, mGluR2/4 dimers were not inhibited by the mGluR2-selective NAM (Z)-1-[2-cycloheptyloxy-2-(2,6-dich

284 Pre-administration of mGluR2-selective PAM, 17 reduced the brain uptake of [(1

285 most vocal nuclei and the group II subtype (mGluR2), showing a unique expression pattern of very low

286 mGluR2 signaling ensures sufficient electrotonic isolati

287 otine exposure could be explained by changed mGluR2 signaling.

288 find that metabotropic glutamate receptor 2 (mGluR2) signaling, which acts on voltage-gated calcium c

289 RGCs) of blind rd1 mice, photoswitch-charged mGluR2 ("SNAG-mGluR2") evoked robust OFF responses to li

290 ssary for the 5-HT(2A)R-dependent effects on mGluR2 subcellular distribution.

291 onist for mGluR1 and a potent antagonist for mGluR2, suggesting that co-recognition of L-glutamate an

292 ted two of the primary neuronal functions of mGluR2: suppression of excitability and inhibition of ne

293 te between the mainly presynaptic inhibitory mGluR2 (the proposed treatment target) and mGluR3.

294 f class C metabotropic glutamate receptor 2 (mGluR2) through a mechanism that required their assembly

295 To date, the target of this non-mGluR2 tracer binding remains unknown.

296 nd deletions revealed that axon exclusion of mGluR2 versus axon targeting of mGluR7 is mediated by th

297 mGluR2 was rapidly, reversibly, and selectively activate

298 concentration = 9.6 nM) for the PAM site of mGluR2, was evaluated as a selective mGluR2 PAM PET trac

299 e used a retinal G protein-coupled receptor, mGluR2, which we chemically engineered to respond to lig

300 ient suppression of synaptic transmission by mGluR2, while enhancing LTD, suggests further that these