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1 dy as a novel antipsychotic therapy aimed at mGluR3.
2 activates a group II metabotropic receptor, mGluR3.
3 re unable to discriminate between mGluR2 and mGluR3.
4 uman mGluR2 and is without activity at human mGluR3.
5 RGT cells transfected with human mGluR2 and mGluR3.
6 RGT cells transfected with human mGluR2 and mGluR3.
7 y mGluR2 (the proposed treatment target) and mGluR3.
11 increasing the duration of NAAG activity on mGluR3 and by reducing degradation into NAA and glutamat
14 s indicate distinct functions for mGluR2 and mGluR3 and suggest a dynamic regulation of mGluR3 by PP2
18 group II metabotropic receptors (mGluR2 and mGluR3) are among different mechanisms that modulate pre
19 e type 1 metabotropic GluR (mGluR1), mGluR2, mGluR3, but not the mGluR5 subtype of G protein-linked m
21 These findings indicate that mGluR2 (but not mGluR3) can selectively modulate GABAergic inhibition in
29 COMT) and in metabotropic glutamate receptor mgluR3 (GRM3), respectively, suggest that these genes in
33 onversely, activation of the Group II mGluR, mGluR3, induces long-term potentiation of electrical syn
35 hat the 50-aa C-terminal cytoplasmic tail of mGluR3 interacts specifically with protein phosphatase 2
39 metabotropic glutamate receptors (mGluR2 and mGluR3) may control relapse of alcohol seeking, but prev
41 Rs (mGluRs), signals for mGluR1, mGluR2, and mGluR3 mRNAs were low or undetectable, whereas mGluR4 an
43 ncrease in GCP II protein and a reduction in mGluR3 protein in the dorsolateral prefrontal cortex in
45 to distinguish the expression of mGluR2 and mGluR3 receptor proteins in schizophrenia and to quantif
47 ed to determine how activation of mGluR2 and mGluR3 receptors (Group II) might modulate visual respon
48 f LY354740 on IPSCs were not mimicked by the mGluR3-selective agonist N-acetyl-aspartyl-glutamate (NA
49 metabotropic glutamate receptors (mGluR2 and mGluR3) were suggested as targets for addiction treatmen
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