蛇毒突触前磷脂酶A_2神经毒素的作用机制研究进展  

Research Advances in the Molecular Mechanism of Snake Presynaptic Phospholipase A_2 Neurotoxins

作　　者：马兆瑞[1] 王振[1] 马亚瑞[2] 何宇[3] 杨章民[1] 

机构地区：[1]陕西师范大学生命科学学院,陕西西安710062 [2]集美大学诚毅学院,福建厦门361021 [3]渭南职业技术学院,陕西渭南714000

出　　处：《安徽农业科学》2012年第13期7749-7751,共3页Journal of Anhui Agricultural Sciences

基　　金：国家自然科学基金(30870303);陕西省自然科学基金(SJ08-C102)

摘　　要：蛇毒突触前磷脂酶A2神经毒素(Snake presynaptic phospholipase A2 neurotoxins,SPANs)是蛇毒中毒性最大的成分之一,主要作用于脊椎动物神经-肌肉接头(Neuromuscular junction,NMJ)处,阻断神经递质乙酰胆碱的释放致使动物肌肉麻痹、呼吸衰竭直至死亡。SPANs与突触前膜特异性结合,水解膜磷脂生成溶血磷脂(Lysophospholipids,LysoPC)和脂肪酸(Fatty acids,FA),改变膜构象、膜通透性提高导致Ca2+大量内流至神经末梢、突触囊泡(Synaptic vesicles,SV)枯竭、线粒体功能障碍等。对蛇毒突触前磷脂酶A2神经毒素的受体分子及其引发的一系列胞内分子事件进行综述。Snake presynaptic phospholipase A2 neurotoxins （SPANs） is the most toxic component of the venom, which causes a persistent blockade of acetyleholine release at vertebrate neuromuscular junctions （NMJ） , leading to muscle paralysis, respiratory failure and ultimately death of the envenomated animal. SPANs bind to the presynaptic membrane specifically and catalyze phospholipid hydrolysis with production of lysophospbolipids （LysoPC） and fatty acids （FA）. These compounds change the membrane conformation and increase the membrane permea- bility to CA2＋ which fluxes from the outside into the nerve terminal. SPANs were shown to induce depletion of synaptic vesicles and mitochon- drial impairment following the production of lysophospholipids and fatty acids. This review gives an introduction about SPANs receptor mole- cules and a series of intracellular molecular events.

关 键 词：蛇毒 磷脂酶A2 突触前神经毒素 分子机制 

分 类 号：S859.8[农业科学—临床兽医学]