Metabotropic Glutamate GPCR Assays
Background of Metabotropic Glutamate Receptors
Metabotropic glutamate receptors (mGluRs) are a large family of glutamate receptors that belongs to the G-protein coupled receptor family. mGluRs can be detected in nearly every important region of the human brain. So far, eight different subtypes of mGluRs (mGlu1-8) have been cloned. mGluRs are subdivided into three groups based on their sequence homology, effector coupling, and pharmacology. Group I mGluRs include mGlu 1 and mGlu 5, they can couple with phospholipase C positively. Group II mGluRs include mGlu 2 and mGlu 3, and the others belong to group III mGluRs. They can both couple to adenylate cyclase negatively.
Fig.1. Structure of the Metabotropic Glutamate receptor 1. (Uniprot ID P23385; obtained from Alphafold)
Distribution and Function of Metabotropic Glutamate Receptors
Metabotropic glutamate receptors are widely distributed throughout the human central nervous (CNS) system and inhibit specifically in discrete synapses of both neurons and glial cells. Their specific distribution locations vary with the group. The activation of group I mGluRs often results in cellular depolarization and increased neuronal excitability. In contrast, group II and group III mGluRs can suppress the release of neurotransmitters.
Subtypes and Mechanisms of Metabotropic Glutamate Receptors
Research on mGluRs and their associated pathways can do great benefit in the treatment of cancer, primary brain tumors, melanoma, and other brain diseases.
| Receptor | Gene | Mechanism | Agonists | Antagonists |
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mGluR1 |
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mGluR2 |
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mGluR3 |
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mGluR4 |
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mGluR5 |
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mGluR6 |
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mGluR7 |
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mGluR8 |
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Assay List of Metabotropic Glutamate Receptors
Creative Biolabs can provide a range of assays of metabotropic glutamate receptors. You can choose the assay in the list or contact us for more information:
Published Data
| Paper Title |
Emotional impairment and persistent upregulation of mGlu5 receptor following morphine abstinence: implications of an mGlu5-MOPr interaction |
| Journal |
International Journal of Neuropsychopharmacology |
| Published | 2016 |
| Abstract |
Opioid addiction is a complex and multi-occurring brain disease. After withdrawal, it will produce various negative emotional conditions including depression, stress, and anxiety, and trigger patients to seek and take drugs compulsively, making the maintenance of a drug-free state extremely difficult. Classical antidepressant medications have not been shown to be effective in this patient population, so addressing the underlying mechanisms of mood disturbance during withdrawal is critical. Previous studies have reported the important role of metabotropic glutamate receptor 5 in opioid administration and withdrawal drug-seeking behavior, especially the involvement of mGlu5R in the process of drug addiction, however, the role of mGlu5R in regulating mood disturbance during morphine withdrawal is not deeply understood. In this study, the researchers evaluated the emotional and behavioral consequences of morphine withdrawal in mice and the reversal effect of mGlu5R on this depression-like behavior. Differences in mGlu5R binding capacity in the mouse brain. The findings demonstrate a critical role of mGlu5R in the central nervous system in modulating negative emotional states during opioid withdrawal and a possible μ-opioid receptor (MOPr)-mGlu5R interaction. |
| Result |
In the experiment, addiction in mice is promoted by seven-day ascending dosing, and the behavior/emotional changes in mice were evaluated by the elevated maze and forced swimming test after withdrawal. mGlu5R binding was assessed by mGlu5R autoradiography in dosed mice, weaned mice, and MOPr knockout mice. Experimental data show that morphine withdrawal leads to emotional and behavioral deficits in mice, as well as a significant neuroadaptive upregulation of mGlu5R binding in the brain. After treatment with mGlu5R antagonists, depression-nourishing behavior is improved and reversed. The binding of mGlu5R in specific regions in the brain of MOPr knockout mice was increased compared with the control group, suggesting that mGlu5R and MOPr may have direct molecular interactions in specific brain regions, and the upregulation of mGlu5R may be caused by MOPr knockout as a compensation mechanism. These results support the possibility of an association of mGlu5R with opioid withdrawal-related affective disorders and the existence of a region-specific MOPr-mGlu5R interaction in the brain.
Fig.2. Morphine |
withdrawal causes changes in mGlu5R binding. (Zanos, 2016)
Reference
- Zanos, P.; et al. Emotional impairment and persistent upregulation of mGlu5 receptor following morphine abstinence: implications of an mGlu5-MOPr interaction. International Journal of Neuropsychopharmacology. 2016, 19(7): 1-10.
