Egea G, Marsal J, Solsona C, Rabasseda X, Blasi J
Departament de Biologia Cellular i Anatomia Patològica, Facultat de Medicina, Hospital de Bellvitge, Universitat de Barcelona, Barcelona, Spain.
Neuroscience. 1989;31(2):521-7. doi: 10.1016/0306-4522(89)90394-1.
We have investigated the redistribution of filipin-cholesterol complexes at freeze-fractured presynaptic membrane of pure cholinergic synaptosomes isolated from Torpedo electric organ during acetylcholine release. After chemical depolarization, filipin-induced lesions increase at the presynaptic membrane. These changes do not take place when synaptosomes are stimulated in a calcium-free medium. Botulinum neurotoxin type A blocks both acetylcholine release and the rearrangement of filipin-induced lesions induced by depolarization. Since botulinum neurotoxin type A does not block either membrane depolarization or calcium entry into the nerve terminal, our results suggest that the redistribution of filipin-cholesterol complexes is linked to the acetylcholine release process.
我们研究了在乙酰胆碱释放过程中,从电鳐电器官分离出的纯胆碱能突触体经冷冻断裂处理后的突触前膜上,制霉菌素-胆固醇复合物的重新分布情况。化学去极化后,突触前膜上制霉菌素诱导的损伤增加。当突触体在无钙培养基中受到刺激时,这些变化不会发生。A型肉毒杆菌神经毒素可阻断乙酰胆碱释放以及去极化诱导的制霉菌素损伤的重排。由于A型肉毒杆菌神经毒素既不阻断膜去极化,也不阻断钙进入神经末梢,我们的结果表明,制霉菌素-胆固醇复合物的重新分布与乙酰胆碱释放过程有关。