Biochemical machinery involved in the release of ATP from sympathetic nerve terminals
Biochemical machinery involved in the release of ATP from sympathetic nerve terminals
复制标题
参与交感神经末梢释放 ATP 的生化机制
DOI：
--
复制
发表时间：
1994
影响因子：
7.3
通讯作者：
T. C. Cunnane
中科院分区：
文献类型：
--
作者：
C. Wardell;T. C. Cunnane
通过细胞内和局灶性细胞外记录技术研究了豚鼠输精管交感神经末梢易化过程的生化机制。phorbol酯，phorbol 12,13 -二丁酸酯（PDBu）对蛋白激酶C的激活极大地增加了序列中第一次刺激的兴奋连接电位（e.j.ps）的振幅，并改变了促进模式。细胞外记录的神经末梢脉冲的结构和结后膜对释放的ATP的敏感性不受影响。特异性蛋白激酶C抑制剂Ro - 31,8220可以消除PDBu的促进和拮抗作用。这些结果表明，蛋白激酶C在交感神经ATP释放中起着重要作用，特别是在促进机制中起着重要作用。
The biochemical mechanisms underlying the process of facilitation in sympathetic nerve terminals of the guinea‐pig vas deferens have been investigated by intracellular and focal extracellular recording techniques. Activation of protein kinase C by the phorbol ester, phorbol 12,13‐dibutyrate (PDBu) greatly increased the amplitude of excitatory junction potentials (e.j.ps) from the first stimulus in a train and altered the pattern of facilitation. The configuration of the extracellularly recorded nerve terminal impulse and the sensitivity of the postjunctional membrane to released ATP were unaffected. The specific protein kinase C inhibitor, Ro‐31,8220, abolished facilitation and antagonized the effects of PDBu. These results suggest that protein kinase C plays a fundamental role in ATP release from sympathetic nerves and in particular in the mechanisms underlying facilitation.