Robitaille R, Charlton M P
Department of Physiology, University of Toronto, Ontario, Canada.
J Neurosci. 1992 Jan;12(1):297-305. doi: 10.1523/JNEUROSCI.12-01-00297.1992.
The regulation of synaptic transmission by Ca(2+)-activated potassium (gKca) channels was investigated at the frog neuromuscular junction (nmj). Charybdotoxin (CTX), a blocker of certain types of gKca channels, induced a twofold increase of transmitter release. Similar results were obtained with purified natural toxin, synthetic toxin, and recombinant toxin. Apamin, a blocker of a different type of gKca channel, did not alter transmitter release. CTX was ineffective after intraterminal Ca2+ buffering was increased by application of the membrane-permeant Ca2+ buffer dimethyl-BAPTA-AM. By itself, the permeant buffer first caused a slight increase in transmitter release before release was eventually decreased. This increase of release did not occur when the buffer was applied in the presence of CTX or Ba2+, another gKca channel blocker. Stimulus-evoked entry of Ca2+ in nerve terminals, detected with the fluorescent Ca2+ indicator FLUO-3, was increased after blockade of gKca channels by CTX. CTX had no effect on the amount or the time course of synaptic depression. The results are consistent with the hypothesis that CTX-sensitive gKca channels normally narrow the presynaptic action potential and thus, by indirectly regulating Ca2+ entry, can serve as powerful modulators of evoked transmitter release. In order to affect presynaptic action potentials, the gKca channels must be located close to Ca2+ channels.
在青蛙神经肌肉接头（nmj）处研究了钙激活钾（gKca）通道对突触传递的调节作用。某些类型gKca通道的阻滞剂蝎毒素（CTX）可使递质释放增加两倍。纯化的天然毒素、合成毒素和重组毒素也得到了类似结果。另一种不同类型gKca通道的阻滞剂蜂毒明肽并未改变递质释放。通过应用膜通透性钙缓冲剂二甲基 - BAPTA - AM增加终末内钙缓冲后，CTX无效。单独使用时，通透性缓冲剂首先会使递质释放略有增加，最终释放量会减少。当在CTX或另一种gKca通道阻滞剂Ba2 +存在的情况下应用缓冲剂时，这种释放增加并未发生。用荧光钙指示剂FLUO - 3检测到，在CTX阻断gKca通道后，刺激诱发的神经末梢钙内流增加。CTX对突触抑制的量或时间进程没有影响。这些结果与以下假设一致：对CTX敏感的gKca通道通常会使突触前动作电位变窄，因此，通过间接调节钙内流，可以作为诱发递质释放的强大调节剂。为了影响突触前动作电位，gKca通道必须位于靠近钙通道的位置。
