Blundon J A, Wright S N, Brodwick M S, Bittner G D
Department of Zoology, University of Texas, Austin 78712.
Proc Natl Acad Sci U S A. 1993 Oct 15;90(20):9388-92. doi: 10.1073/pnas.90.20.9388.
An increase in internal free calcium ([Ca2+]i) in the presynaptic terminal is often assumed to directly produce facilitation of neurotransmitter release. Using a Ca(2+)-activated potassium conductance as a bioassay for free [Ca2+]i in the presynaptic terminal of the crayfish (Procambarus clarkii) opener neuromuscular junction, we now demonstrate that free [Ca2+]i has a decay time constant (tau) of 1-4 msec, whereas facilitation of neurotransmitter release has a decay tau of 7-43 msec. In addition, facilitation of neurotransmitter release can be markedly different at times when free [Ca2+]i values and presynaptic membrane voltages are equal. We conclude that free [Ca2+]i in the presynaptic terminal is not directly responsible for facilitation of neurotransmitter release. Our data suggest that facilitation results from bound Ca2+ or some long-lived consequence of bound Ca2+.
通常认为，突触前终末内的游离钙（[Ca2+]i）增加会直接导致神经递质释放的易化。我们利用一种钙激活钾电导作为小龙虾（克氏原螯虾）开肌神经肌肉接头突触前终末游离[Ca2+]i的生物测定方法，现证明游离[Ca2+]i的衰减时间常数（tau）为1 - 4毫秒，而神经递质释放的易化具有7 - 43毫秒的衰减tau。此外，当游离[Ca2+]i值和突触前膜电压相等时，神经递质释放的易化在不同时间可能会有显著差异。我们得出结论，突触前终末内的游离[Ca2+]i并非直接导致神经递质释放的易化。我们的数据表明，易化是由结合钙或结合钙的某些长时效应引起的。
