SUPPRESSION OF LTD IN CULTURED PURKINJE-CELLS DEFICIENT IN THE GLUTAMATE-RECEPTOR DELTA-2 SUBUNIT
SUPPRESSION OF LTD IN CULTURED PURKINJE-CELLS DEFICIENT IN THE GLUTAMATE-RECEPTOR DELTA-2 SUBUNIT
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DOI：
10.1097/00001756-199502000-00029
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发表时间：
1995-02-15
期刊：
影响因子：
1.7
通讯作者：
MISHINA, M
中科院分区：
文献类型：
--
作者：
HIRANO, T;KASONO, K;MISHINA, M
研究了谷氨酸受体通道德尔塔2亚基缺失的野生型和突变小鼠在小脑长期抑郁(LTD)中的作用。LTD的谷氨酸反应是通过配对谷氨酸应用和野生型培养中浦肯野细胞的去极化诱导的。然而，在从突变小鼠制备的培养浦肯野细胞中，同样的条件未能诱导LTD。免疫细胞学染色显示，突变的浦肯野细胞与野生型细胞一样，发育并表达钙结合蛋白(浦肯野细胞的标志蛋白)，但它们不表达Delta 2亚单位蛋白。结果表明，谷氨酸受体通道德尔塔2亚单位参与了突触后谷氨酸敏感性的下调，可能发生在小脑LTD。
INVOLVEMENT of the glutamate receptor channel delta 2 subunit in cerebellar long-term depression (LTD) was studied in cultures prepared from wild-type and mutant mice deficient in the delta 2 subunit. LTD of the glutamate response was induced by pairing glutamate applications and depolarization of a Purkinje cell in wild-type culture. However, in cultured Purkinje cells prepared from mutant mice, the same conditioning failed to induce LTD. Immunocytological staining showed that mutant Purkinje cells develop and express calbindin (a marker protein for Purkinje cells) as do wild-type cells, but they express no delta 2 subunit protein. The results indicate that the glutamate receptor channel delta 2 subunit is involved in the postsynaptic downregulation of glutamate sensitivity, presumably during cerebellar LTD.