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机构地区:[1]第二军医大学生理学教研室,上海200433 [2]中国科学院上海细胞生物学研究所,上海200031
出 处:《生理学报》1998年第3期345-348,共4页Acta Physiologica Sinica
摘 要:采用大鼠大脑皮层突触体、人神经母细胞瘤细胞株SK-N-SH及人多形胶质瘤细胞株BT-325作氚标谷氨酸高亲和摄取实验,探讨蛋白激酶C(PKC)及蛋白激酶A(PKA)对于神经元性及胶质细胞性谷氨酸(Glu)摄取的影响。结果:(1)PKC激活剂(PMA,佛波醇之一种)对于突触体及BT-325细胞摄取Glu有促进作用,但对于SK-N-SH摄取Glu没有影响;PKC抑制剂(SPH)能抑制PMA的促进效应。(2)PKA激活剂(db-cAMP)对于突触体、SK-N-SH及BT-325细胞摄取Glu均无影响。这些结果表明PKC对于胶质细胞性Clu摄取可能具有促进作用,而对于神经元性Glu摄取不排除有一定影响的可能;PKA对于Glu摄取(包括神经元性及胶质细胞性)没有影响。The effects of protein kinase C (PKC) and protein kinase A (PKA) on the high affinity glutalnate uptake in rat cerebral cortex synaptosomesg cell lines of human neuroblastorna SK-N-SH and human anaplastic astrocytoma BT-325 were studied by measurement of radioactivity of 3 [H] -L-glutarnate. The results were as follows: (1)PKC agonist phorbol-12-myristate, 13-acetate (PMA) stimulated the glutamate uptake in foe rat cerebral cortex synaptosomes and cell line of BT-325, but not in the cell line of SK-N-SH. This effect of PMA was abolished in the presence of PKC antagonist sphingosine. (2) Glutarnate uptake in all these three samples of neural tissues and cells was not edicted by PKA agonist adenosine 3', 5 1 - cycli cmonopho sphate, N6, O2' dibutyryl. The above results indicate that it is PKC that stimulates high sanity glutamate uptake in glial cells, although the possibility that neurons are also affected to some extent can not be mied out.
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