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纹状体突触体中钾离子依赖性多巴胺合成的刺激是由蛋白激酶C介导的。

K+-dependent stimulation of dopamine synthesis in striatal synaptosomes is mediated by protein kinase C.

作者信息

Chowdhury M, Fillenz M

机构信息

University Laboratory of Physiology, Oxford, England.

出版信息

J Neurochem. 1988 Feb;50(2):624-9. doi: 10.1111/j.1471-4159.1988.tb02956.x.

Abstract

Dopamine synthesis rate was measured in striatal synaptosomes. Removal of Na+ increased synthesis rate; this was blocked in Ca2+-free medium and by addition of the Ca2+/calmodulin inhibitor N-6-aminohexyl-5-chloro-1-naphthalenesulfonamide (W7). The increase in dopamine synthesis rate caused by the addition of the phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA) was blocked by the protein kinase C inhibitor polymyxin B. K+-stimulated synthesis was unchanged in Ca2+-free medium or by addition of W7; it was blocked by polymyxin B. The effect of 50 mM K+ was additive with that of 8-Br cyclic AMP and of Na+ removal; the combined effect of 50 mM K+ and TPA was no greater than that of either alone. These results suggest that stimulation of dopamine synthesis in striatal synaptosomes by 50 mM K+ is mediated by protein kinase C.

摘要

在纹状体突触体中测量多巴胺合成速率。去除Na+会增加合成速率;在无Ca2+的培养基中以及添加Ca2+/钙调蛋白抑制剂N-6-氨基己基-5-氯-1-萘磺酰胺(W7)时,这种增加被阻断。添加佛波酯12-O-十四酰佛波醇-13-乙酸酯(TPA)引起的多巴胺合成速率增加被蛋白激酶C抑制剂多粘菌素B阻断。在无Ca2+的培养基中或添加W7时,K+刺激的合成没有变化;它被多粘菌素B阻断。50 mM K+的作用与8-溴环磷酸腺苷和去除Na+的作用相加;50 mM K+和TPA的联合作用不大于单独任何一种的作用。这些结果表明,50 mM K+对纹状体突触体中多巴胺合成的刺激是由蛋白激酶C介导的。

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