Noremberg K, Parsons S M
J Neurochem. 1986 Oct;47(4):1312-7. doi: 10.1111/j.1471-4159.1986.tb00756.x.
The total fatty acid composition of purified Torpedo californica electric organ synaptic vesicles was determined by GLC analysis of methyl esters. Limit amounts of fatty acids released by high concentrations of either beta-bungarotoxin (beta-BuTx) or Naja naja venom phospholipase A2 (PLA2) acting in deoxycholate are reported. The time and enzyme concentration dependence for beta-BuTx- and PLA2-induced release of fatty acids from intact synaptic vesicles indicate that PLA2 is 100- to 1,000-fold more active. The Ca2+ dependence for beta-BuTx-induced release of fatty acids also was determined. ATP inhibits beta-BuTx- but not PLA2-induced release of fatty acids from vesicles in a manner that can not be ascribed only to chelation of the required Ca2+. ATP, other nucleotides, and adenosine have complex effects on beta-BuTx-induced release of fatty acids from egg yolk phosphatidylcholine dispersed in deoxycholate. The results suggest that beta-BuTx-mediated hydrolysis of the cholinergic synaptic vesicle membrane is approximately 10- to 100-fold more effective at causing uncoupling of vesicles than is PLA2 and that the enzymatic activity of beta-BuTx is subject to regulation by nucleotide-like factors.
通过对甲酯进行气相色谱分析，确定了纯化的加州电鳐电器官突触小泡的总脂肪酸组成。报告了在脱氧胆酸盐存在下，高浓度的β-银环蛇毒素（β-BuTx）或眼镜蛇毒磷脂酶A2（PLA2）释放的脂肪酸限量。β-BuTx和PLA2诱导完整突触小泡释放脂肪酸的时间和酶浓度依赖性表明，PLA2的活性高100至1000倍。还确定了β-BuTx诱导脂肪酸释放的Ca2+依赖性。ATP以一种不能仅归因于所需Ca2+螯合的方式抑制β-BuTx诱导的小泡脂肪酸释放，但不抑制PLA2诱导的释放。ATP、其他核苷酸和腺苷对分散在脱氧胆酸盐中的蛋黄磷脂酰胆碱中β-BuTx诱导的脂肪酸释放有复杂影响。结果表明，β-BuTx介导的胆碱能突触小泡膜水解在导致小泡解偶联方面比PLA2有效约10至100倍，并且β-BuTx的酶活性受核苷酸样因子的调节。
