| First Author | Li J | Year | 2002 |
| Journal | Mol Cell Neurosci | Volume | 19 |
| Issue | 2 | Pages | 138-51 |
| PubMed ID | 11860268 | Mgi Jnum | J:75442 |
| Mgi Id | MGI:2176635 | Doi | 10.1006/mcne.2001.1085 |
| Citation | Li J, et al. (2002) Reduced Cortical Synaptic Plasticity and GluR1 Expression Associated with Fragile X Mental Retardation Protein Deficiency. Mol Cell Neurosci 19(2):138-51 |
| abstractText | Lack of expression of the fragile X mental retardation protein (FMRP), due to silencing of the FMR1 gene, causes the Fragile X syndrome. Although FMRP was characterized previously to be an RNA binding protein, little is known about its function or the mechanisms underlying the Fragile X syndrome. Here we report that the alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate receptor subunit, GluR1, was decreased in the cortical synapses, but not in the hippocampus or cerebellum, of FMR1 gene knockout mice. Reduced long-term potentiation (LTP) was also found in the cortex but not in the hippocampus. Another RNA binding protein, FXR; the N-methyl-d-aspartate receptor subunit, NR2; and other learning-related proteins including c-fos, synapsin, myelin proteolipid protein, and cAMP response element binding protein were not different between FMR1 gene knockout and wild-type mice. These findings suggest that the depressed cortical GluR1 expression and LTP associated with FMRP deficiency could contribute to the Fragile X phenotype. (C)2002 Elsevier Science (USA). |
