Garrett K M, Ross D H
Neurochem Res. 1983 Aug;8(8):1013-28. doi: 10.1007/BF00965197.
Acute administration of ethanol (4 g/kg, i.p.) to mice inhibits the sequestration of calcium into endoplasmic reticulum-like organelles in synaptosomal membranes. Ethanol administration inhibits both Ca2+-stimulated adenosine triphosphate hydrolysis and ATP-dependent calcium uptake in the vesicles at time of loss of righting reflex. At recovery of righting reflex, the Ca2+-ATPase activity returns to normal levels, while the ATP-dependent uptake remains inhibited. The effect of ethanol is specific for the sequestration (active transport) of calcium since calcium binding to synaptic membranes is not altered. Alteration in mechanisms responsible for synaptosomal buffering of cytosolic Ca2+ levels by in vivo ethanol may contribute to altered transmitter release rates following ethanol administration.
给小鼠腹腔注射乙醇(4克/千克)可抑制钙在突触体膜内内质网样细胞器中的隔离。在翻正反射消失时,乙醇给药会抑制囊泡中Ca2+刺激的三磷酸腺苷水解和ATP依赖的钙摄取。在翻正反射恢复时,Ca2+-ATP酶活性恢复到正常水平,而ATP依赖的摄取仍受抑制。乙醇的作用对钙的隔离(主动转运)具有特异性,因为钙与突触膜的结合没有改变。体内乙醇改变负责突触体缓冲胞质Ca2+水平的机制,可能导致乙醇给药后递质释放速率改变。