论文部分内容阅读
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。
Using rat cerebral cortex synaptosome, human neuroblastoma cell line SK-N-SH and human pleomorphic glioma cell line BT-325 as tritiated glutamate high affinity uptake experiments to explore the protein kinase C ( PKC) and protein kinase A (PKA) on neuronal and glial glutamate uptake. Results: (1) PKC activator (PMA, a kind of phorbol) promoted Glu uptake in synaptosomes and BT-325 cells, but had no effect on Glu uptake by SK-N-SH. PKC inhibitor ) Can inhibit the promotion effect of PMA. (2) PKA activator (db-cAMP) had no effect on the uptake of Glu in synaptosomes, SK-N-SH and BT-325 cells. These results indicate that PKC may promote the uptake of glial Clu, but not for neuronal Glu uptake. PKA has no effect on Glu uptake, including neuronal and glial cell.