| First Author | Fukamauchi F | Year | 2001 |
| Journal | Biochem Biophys Res Commun | Volume | 281 |
| Issue | 1 | Pages | 220-6 |
| PubMed ID | 11178983 | Mgi Jnum | J:67556 |
| Mgi Id | MGI:1930847 | Doi | 10.1006/bbrc.2001.4334 |
| Citation | Fukamauchi F, et al. (2001) TAG-1-deficient mice have marked elevation of adenosine A1 receptors in the hippocampus. Biochem Biophys Res Commun 281(1):220-6 |
| abstractText | TAG-1 is a neural recognition molecule in the immunoglobulin superfamily that is predominantly expressed in the developing brain. Several lines of evidence suggest that TAG-1 is involved in the outgrowth, guidance, and fasciculation of neurites. To directly assess the function of TAG-1 in vivo, we have generated mice with a deletion in the gene encoding TAG-1 using homologous recombination in embryonic stem cells. Gross morphological analysis of the cerebellum, the spinal cord, and the hippocampus appeared normal in TAG-1-deficient mice. However, TAG-1 (-/-) mice showed the upregulation of the adenosine A1 receptors determined by [(3)H]cyclopentyl-1,3-dipropylxanthine in the hippocampus, and their greater sensitivity to convulsant stimuli than that in TAG-1 (+/+) mice. We suspect that the subtle changes in neural plasticity induced by TAG-1 deficiency during development cause the selective vulnerability of specific brain regions and the epileptogenicity in TAG-1 (-/-) mice. |
