TAG-1-deficient mice have marked elevation of adenosine A1 receptors in the hippocampus
TAG-1-deficient mice have marked elevation of adenosine A1 receptors in the hippocampus
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DOI：
10.1006/bbrc.2001.4334
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发表时间：
2001-02-16
影响因子：
3.1
通讯作者：
Iwakura, Y
中科院分区：
文献类型：
--
作者：
Fukamauchi, F;Aihara, O;Iwakura, Y
TAG-1是免疫球蛋白超家族中的神经识别分子，主要在发育中的大脑中表达。几条证据表明TAG-1参与神经突的生长、引导和成束。为了直接评估TAG-1在体内的功能，我们使用胚胎干细胞中的同源重组产生了TAG-1编码基因缺失的小鼠。TAG-1缺陷小鼠的小脑、脊髓和海马的大体形态学分析显示正常。然而，TAG-1（-/-）小鼠表现出海马中腺苷A1受体的上调（由[H-3]环戊基-1，3-二丙基黄嘌呤测定），并且它们比TAG-1（+/+）小鼠对惊厥刺激更敏感。我们推测，TAG-1缺陷引起的发育过程中神经可塑性的微妙变化导致了TAG-1（-/-）小鼠特定脑区的选择性脆弱性和致癫痫性。(C)北京：科学出版社.
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 Al receptors determined by [H-3]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. (C) 2001 Academic Press.