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1 n for the metabotropic glutamate receptor 7 (mGluR7).
2  by sensory activity, in contrast to that of mGluR7.
3 uR1, and the group III receptors, mGluR4 and mGluR7.
4 ty of orthosteric and allosteric agonists at mGluR7.
5 subunits mGluR1, mGluR3, mGluR4, mGluR5, and mGluR7.
6 mGluR1 alpha, mGluR2/3, mGluR4a, mGluR5, and mGluR7.
7 Ser(862) or the regulation of CaM binding to mGluR7.
8 eractions with the carboxyl-terminal tail of mGluR7.
9 kinase-mediated inhibition of CaM binding to mGluR7.
10 ts in the ligand binding domain (LBD) of the mGluR7/7 homodimer revealed it to have an apparent affin
11 y for the metabotropic glutamate receptor 7 (mGLUR7), a SUMO-enriched protein in the mass spectrometr
12                             In naive slices, mGluR7 activation during HFS generates MF-SLIN LTD, depr
13                                              mGluR7 activation during high-frequency stimulation (HFS
14 immunocytochemical results demonstrated that mGluR7 activation increased cofilin activity and F-actin
15 Fil VGCC depression results from HFS-induced mGluR7 activation leading to persistent P/Q-type VGCC in
16 mGluR7-RIM1alpha interaction is regulated by mGluR7 activation, and mice lacking RIM1alpha are defici
17                                      Rather, mGluR7 activation/internalization controls plasticity po
18 ansmission has been shown to be modulated by mGluR7 activity.
19    We also discovered an association between mGluR7 and RIM1alpha, an active zone molecule required f
20 um mobilization assays in cells coexpressing mGluR7 and the promiscuous G protein G alpha(15).
21 ession of metabotropic glutamate receptor 7 (mGluR7) and presynaptic GluK2-containing kainate recepto
22 ted the in vitro characterization of a novel mGluR7 antagonist called 6-(4-methoxyphenyl)-5-methyl-3-
23 ximal dendrites were strongly labeled by the mGluR7 antibody.
24                           Distinct levels of mGluR7 are found at different synapses made by individua
25 aled that immunoreactivities for mGluR4a and mGluR7 are widely but differentially distributed through
26 -, PKA-, or PKG-dependent phosphorylation of mGluR7 at a single serine residue, Ser(862), in the carb
27    However, the postsynaptic localization of mGluR7 at selected synapses indicates that mGluR7 is not
28                              The presence of mGluR7 at these multiple sites in the basal ganglia sugg
29 ry input by whisker trimming does not affect mGluR7 but prevents the emergence of presynaptic GluK2-K
30                      These data suggest that mGluR7, by affecting the cofilin/actin signaling, regula
31                              Addition of the mGluR7 C-terminal sequence to mGluR2 or to the unrelated
32 ibits kinase-mediated phosphorylation of the mGluR7 carboxyl terminus and reverses kinase-mediated in
33  transsynaptic interaction between Elfn1 and mGluR7 constitutively reduces initial release probabilit
34 R1a, mGluR2, and D2 were comparable, whereas mGluR7 currents were somewhat smaller.
35                                          The mGluR7 cytoplasmic domain appended to the transmembrane
36                            Truncation of the mGluR7 cytoplasmic tail produces a protein that is restr
37 n and surface expression are diminished, and mGluR7-dependent plasticity at mossy fiber-interneuron h
38                                              mGluR7 differs from mGluR4 and other group III mGluR in
39 horylation and inhibit CaM interactions with mGluR7 does not affect receptor function.
40 ated that mutating this residue to lysine in mGluR7 enhances the potency of L-SOP.
41                          While naive surface mGluR7 expressing MF-SLIN synapses are insensitive to cA
42  we find that removal of both GluK2-KARs and mGluR7 from the synapse eliminates short-term facilitati
43                                              mGluR7 has low affinity and efficacy for activation by b
44 opic glutamate receptors (mGluRs) mGluR4 and mGluR7 have been postulated to serve as presynaptic auto
45                                     However, mGluR7 heterodimerizes, and we find it to associate with
46                                       Strong mGluR7 hybridization signals are found in cerebral corte
47 aining was most abundant in IPL sublamina 1; mGluR7 immunoreactivity was organized in four bands, cor
48 compounds differentially inhibit coupling of mGluR7 in different cellular backgrounds and may not ant
49 tial mechanism for understanding the role of mGluR7 in mental health and disorders.
50 ng bulbectomy, consistent with expression of mGluR7 in mitral cell axon terminals.
51 sis of this region confirmed the presence of mGluR7 in multiple axon terminals.
52 es of mGluRs: mGluRla, mGluR2/3, mGluR5, and mGluR7 in the dorsal and ventral autonomic nuclei of the
53 onsistent with a largely presynaptic role of mGluR7 in the hippocampus and suggest that mGluR4 may ha
54     To investigate the immunolocalization of mGluR7 in the olfactory system, we used a polyclonal ant
55 show that a metabotropic glutamate receptor (mGluR7) in the rat hippocampus is restricted to the pres
56                           However, following mGluR7 internalization HFS produces presynaptic LTP.
57 l studies in human and mouse and showed that mGluR7 is expressed in hair cells and in spiral ganglion
58 exclusion of mGluR2 versus axon targeting of mGluR7 is mediated by their 60 amino acid C-terminal cyt
59         Thus, the cytoplasmic tail domain of mGluR7 is necessary but not sufficient for polarized tar
60 f mGluR7 at selected synapses indicates that mGluR7 is not targeted exclusively to axonal compartment
61                    Our results indicate that mGluR7 is primarily presynaptic at olfactory bulb synaps
62 o dendrites and excluded from axons, whereas mGluR7 is targeted to axons and dendrites.
63 t metabotropic glutamate receptor subtype 7 (mGluR7) is a metaplastic switch at MF-SLIN synapses, who
64                          Because ablation of mGluR7 leads to a variety of behavioral symptoms related
65 AMPA receptors and activation of presynaptic mGluR7-like receptors.
66                                        Thus, mGluR7 localization to MF-SLIN terminals and not MFBs al
67 PFC pyramidal neurons, which was mediated by mGluR7 localized at postsynaptic neurons and involved th
68 econd messenger-dependent kinases to inhibit mGluR7-mediated activation of GIRK current is not depend
69 suggest that CaM binding is not required for mGluR7-mediated activation of GIRK current.
70 ment of two separate presynaptic components: mGluR7 (metabotropic glutamate receptor 7) and GluK2-KAR
71 onding to lysine in mGluR4 and asparagine in mGluR7 might play a key role, and, indeed, mutagenesis e
72 ptic metabotropic glutamate receptor (mGluR) mGluR7 modulates excitatory neurotransmission by regulat
73                                          The mGluR7 modulation of NMDAR currents was prevented by age
74     We have examined the localization of the mGluR7 mRNA and mGluR7a protein in the basal ganglia of
75 eled the previously reported distribution of mGluR7 mRNA.
76 identified by computational docking produced mGluR7 mutants that respond with dramatically enhanced p
77 al mechanisms are likely required to mediate mGluR7 neuronal polarization and synaptic clustering.
78                           Phosphorylation of mGluR7 on serine 862 (S862) inhibits CaM binding, thereb
79 KC phosphorylation act together to stabilize mGluR7 on the cell surface in vivo.
80 ce lacking PICK1, PKC-dependent increases in mGluR7 phosphorylation and surface expression are dimini
81 g glutamate release through infusions of the mGluR7 presynaptic receptor antagonist MMPIP had no effe
82 terneurons are mediated by both constitutive mGluR7 recruitment and regulated GluK2 kainate receptor
83 nterneurons is mediated both by constitutive mGluR7 recruitment by Elfn1 and regulated GluK2-KAR recr
84                                 Furthermore, mGluR7 reduced the association of NMDARs with the scaffo
85 tivated STAT1 (Pias1), which can SUMO modify mGLUR7, reduced this Huntington's disease phenotype.
86                         Immunoreactivity for mGluR7 revealed largely presynaptic localization of this
87                             Importantly, the mGluR7-RIM1alpha interaction is regulated by mGluR7 acti
88 ate-dependent cAMP sensitivity controlled by mGluR7-RIM1alpha interactions underlies MF-SLIN metaplas
89 P elevation, synapses that have internalized mGluR7 robustly potentiate following cAMP increases.
90         lucidum interneuron (SLIN) synapses, mGluR7 serves as a metaplastic switch controlling bidire
91  GPCR activity through a transsynaptic Elfn1/mGluR7 structural interaction.
92 g metabotropic glutamate receptor subtype 7 (mGluR7) suggest that antagonists of this receptor may be
93 62) inhibits CaM binding, thereby increasing mGluR7 surface expression and receptor binding to PICK1.
94           Although the dynamic regulation of mGluR7 surface expression governs a form of metaplastici
95                             We now show that mGluR7 surface expression is stabilized by both PKC phos
96                              Thus, selective mGluR7 targeting to MF terminals contacting SLINs and no
97 least a ten-fold higher level of presynaptic mGluR7 than terminals making synapses with pyramidal cel
98 ted inhibition of the functional coupling of mGluR7 to G protein-coupled inward rectifier potassium (
99 wn about the molecular mechanisms regulating mGluR7 trafficking.
100                  Following agonist exposure, mGluR7 undergoes internalization, unmasking the ability
101 ent synaptic components (both GluK2-KARs and mGluR7 via Elfn1 deletion) contributes to a decrease in
102 produces glutamate-independent activation of mGluR7 via presynaptic clustering, resulting in a diverg
103                                 In contrast, mGluR7 was expressed primarily in fibers and terminals i
104                         Immunoreactivity for mGluR7 was variable in different brain regions and close
105               mGluR2/3, mGluR4a, mGluR5, and mGluR7 were also expressed in meningeal microvasculature
106 ntrast, mGluR1 alpha, mGluR2/3, mGluR4a, and mGluR7 were expressed in leptomeninges from adult rats.
107            Instead, we found that mGluR4 and mGluR7 were located close to bipolar cell ribbons.
108 dies that specifically react with mGluR4a or mGluR7 were produced and used for immunocytochemical loc
109 b express mRNA for several mGluRs, including mGluR7, which has been suggested as a presynaptic glutam
110 teractions of presynaptic mGluRs, especially mGluR7, with multiple protein kinases and putative regul

 
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