Basic information of Gria3 :
| Official Symbol of Gene | Gria3 |
| Species | Mus musculus |
| Entrez Gene ID | 53623 |
| Official Full Name | glutamate receptor, ionotropic, AMPA3 (alpha 3) |
| Also known as | GluA3; Glur3; GluR-C; Glur-3; GluR-K3; Gluralpha3; 2900064I19Rik |
| Gene Type | protein coding |
| dbXrefs | Ensembl:ENSMUSG00000001986 AllianceGenome:MGI:95810 |
| Map Location | X A4; X 23.19 cM |
| Variation Type | Deletion |
| refSNP ID | N/A |
Sample information of multiple sclerosis:
| Detected Sample | CNS tissues |
| Sample Detail | N/A |
| Detected Method | quantitative reverse transcriptase-PCR |
| Disease | EAE |
| Disease subtype | N/A |
| Population | C57BL6 mice |
| Sample Size | N/A |
Literature information of multiple sclerosis :
| Pubmed ID | 17472701 |
| Year | 2007 |
| Title | GluR2-free alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate receptors intensify demyelination in experimental autoimmune encephalomyelitis |
Results of multiple sclerosis :
| Risk Type | Disease risk |
| Main Result | Positive |
| Result | Disruption of the Gria3 gene did not induce compensatory changes in levels of mRNAs encoding GluR1, GluR2, or GluR4 in mouse spinal cord or cerebellum, but GluR1 mRNA was significantly elevated in Gria3 mutant cerebral cortex.GluR2-free AMPA receptor-mediated currents are markedly diminished in Gria3-deficient OLC.Whole-cell capacitances of Gria3 mutant and control OLC, did not differ significantly.Block of AMPA receptor currents by NASPM is less in Gria3 mutant (Gria3 KO) than in wild-type (WT) control OLC. OLC from Gria3 mutant mice was less susceptible than control OLC to excitotoxic death.Experimental autoimmune encephalomyelitis clinical deficits and spinal cord demyelination are less severe in Gria3 mutant mice than in wild-type littermate controls. |
| Mechanism/Pathway | This use-dependence has been attributed to a greater accessibility of the polyamine toxin to its interaction site in the agonist-bound, open state of GluR2-lacking AMPA receptors, resulting in an attenuated initial response shortened and further attenuated by the progressive block by the toxin as it enters the opened pores of the channels.OLC excitotoxicity mediated by GluR2-free, Ca2+- permeable AMPA receptors contributes substantially to clinical deficits and demyelination in EAE. |
