GRM3 Membrane Protein Introduction

Introduction of GRM3

GRM3 (mGluR3) belongs to group II receptors of metabotropic glutamate receptors (mGluRs), which are coupled to G_i/o. mGluRs are members of the family C G-protein coupled receptors (GPCRs) and play central roles in neuronal excitation in the central nervous system. Like GRM2, GRM3 modulates neuronal excitability by regulating glutamate (and GABA) release from presynaptic terminals, and postsynaptically by regulating the activity of adenylate cyclase and various ion channels. Structurally, GRM3 has a large extracellular domain, which is a main characteristic of the family C GPCRs and is capable of binding glutamate, transmitting signals through the receptor protein to intracellular signaling partners. GRM3 is widely expressed in neurons and glia with high expression in the cerebral cortex, hippocampus, thalamus, striatum andsubstantianigra.

Functions of GRM3 Membrane Protein

The functions of GRM3 mainly stem from knockout mice. Behavioral studies of mice lacking GRM3 suggested a role of this receptor in anxiety behaviors. Moreover, polymorphisms in the GRM3 encoding gene GRM3 have been linked to schizophrenia and cognitive performance in humans. Thus, the agonist, antagonist and allosteric modulator drugs of GRM3 can now be explored as new treatments for a variety of mental illness. LY354740 and LY379268 are two potent and highly selective agonists of group II mGluRs (mGluR2 and mGluR3), which are used to provide insight into the in vitro and in vivo functional studies of these receptors. Moreover, LY379268 has been found to attenuate extinction latencies and the reinstatement of morphine-induced conditioned place preference in rats.

Applications of GRM3 Membrane Protein in Literature

1. Walker A. G., et al. Co-activation of metabotropic glutamate receptor 3 and beta-adrenergic receptors modulates cyclic-AMP, long-term potentiation, and disrupts memory reconsolidation. Neuropsychopharmacology Official Publication of the American College of Neuropsychopharmacology. 2017, 42(13): 2553. PubMed ID: 28664928
   
   

   This article utilized novel mGluRsubtype-specific allosteric modulators and knockout mice to show that the mGluR3 was responsible for potentiating βAR-elicited cAMP responses in brain slices.

2. OlszewskiR. T., et al. NAAG peptidase inhibitors act via mGluR3: animal models of memory, Alzheimer's, and ethanol intoxication. Neurochemical Research. 2017, 42(9): 2646-2657. PubMed ID: 28285415
   
   

   This article investigated the mechanisms of GCPII inhibitors in animal models of memory and memory loss. The data supported that inhibitors of GCPII were efficacious in object recognition models of normal memory and memory deficits via mGluR3 mediated process.

3. Lainiola M., et al. mGluR3 knockout mice show a working memory defect and an enhanced response to MK-801 in the T- and Y-maze cognitive tests. Behavioural Brain Research. 2014, 266(11): 94-103. PubMed ID: 24631392
   
   

   This study showed that the genetic deletion of mGluR3 caused significantly reduced spontaneous alternation and the application of MK-801enhanced locomotion more than wild type mice.

4. Miyamoto Y., et al. Striatal N-acetylaspartatesynthetaseShati/Nat8l regulates depression-like behaviors via mGluR3-mediated serotonergic suppression in mice. Int J Neuropsychopharmacol. 2017, 20(12): 1027-1035. PubMed ID: 29020418
   
   

   This finding indicated that the striatal expression of N-acetylaspartatesynthetaseShati/Nat8l played a role in major depressive disorder via the mGluR3-mediated functional control of the serotonergic neuronal system.

5. Neto A and Ceol C J. Melanoma-associated GRM3 variants dysregulatemelanosome trafficking and cAMP signaling. Pigment Cell & Melanoma Research. 2017. PubMed ID: 28646617
   
   

   This article studies the tumor-associated variants of the mutated GRM3 gene and found that the oncogenic properties of GRM3 could be mediated, at least in part, by alterations in cAMP signaling.

GRM3 Preparation Options

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