ライフサイエンスコーパス: mGluR2

1 metabotropic glutamate subtype 2 receptors (mGluR2).

2 from R1a increased the surface stability of mGluR2.

3 h the reported intracerebral distribution of mGluR2.

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

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

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

7 y a mutation that disrupts the gene encoding mGluR2.

8 that leads to largely uncompensated loss of mGluR2.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

33 The mGluR2/3 antagonist LY341495 blocked these behavioral an

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

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

36 A unique pattern of staining was found with mGluR2/3 antibody--with staining concentrated in Golgi c

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

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

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

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

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

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

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

44 rose reinstatement was potentiated following mGluR2/3 blockade.

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

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

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

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

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

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

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

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

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

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

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

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

57 mGluR2/3 immunoreactivity was mainly localized in astroc

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

59 mGluR2/3 immunostaining was distributed only in the neur

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

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

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

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

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

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

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

67 Examination of brain sections stained for mGluR2/3 is consistent with this notion, with many cells

68 Strong immunoreactivity for mGluR2/3 is found in cells in the optic pathway and thal

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

149 SAR218645 potentiated mGluR2 agonist-induced contralateral turning.

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

151 ]20f binds specifically and reversibly to an mGluR2 allosteric site, strongly suggesting that it is a

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

153 itional D2 receptor current, indicating that mGluR2 and D2 receptor coupling to GIRK involves a commo

154 In oocytes in which mGluR2 and D2 were coexpressed, activation of mGluR2 occ

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

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

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

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

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

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

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

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

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

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

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

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

167 agonists were unable to discriminate between mGluR2 and mGluR3.

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

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

170 ansmission at parallel fiber synapses, while mGluR2 and/or mGluR3 may modulate mossy terminal functio

171 The current amplitudes evoked by mGluR1a, mGluR2, and D2 were comparable, whereas mGluR7 currents

172 botropic GluRs (mGluRs), signals for mGluR1, mGluR2, and mGluR3 mRNAs were low or undetectable, where

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

188 SNAG-mGluR2 enabled animals to discriminate parallel from per

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

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

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

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

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

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

195 the precise mechanism by which PKA inhibits mGluR2 function.

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

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

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

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

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

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

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

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

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

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

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

207 29 potentiated agonist-induced activation of mGluR2 in the membrane-binding assay and in primate cort

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

225 Furthermore, mGluR2-mediated dendritic compartmentalization in SACs i

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

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

228 Expression of mGluR2 metabotropic glutamate receptors, another pertuss

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

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

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

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

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

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

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

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

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

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

239 GluR2 and D2 were coexpressed, activation of mGluR2 occluded additional D2 receptor current, indicati

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

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

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

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

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

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

246 mGluR2 participates in at least three types of mossy fib

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

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

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

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

251 mGluR2 receptor expression was absent, synaptic glutamat

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

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

254 of LY487379 potentiated synaptically evoked mGluR2 responses.

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

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

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

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

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

260 mGluR2 signaling ensures sufficient electrotonic isolati

261 otine exposure could be explained by changed mGluR2 signaling.

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

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

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

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

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

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

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

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

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

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