Warbington L, Hillman T, Adams C, Stern M
Department of Biochemistry and Cell Biology, Rice University, Houston, TX 77251, USA.
Invert Neurosci. 1996 Jun;2(1):51-60. doi: 10.1007/BF02336660.
Potassium channels control the repolarization of nerve terminals and thus play important roles in the control of synaptic transmission. Here we describe the effects of mutations in the slowpoke gene, which is the structural gene for a calcium activated potassium channel, on transmitter release at the neuromuscular junction in Drosophila melanogaster. Surprisingly, we find that the slowpoke mutant exhibits reduced transmitter release compared to normal. Similarly, the slowpoke mutation significantly suppresses the increased transmitter release conferred either by a mutation in Shaker or by application of 4-aminopyridine, which blocks the Shaker-encoded potassium channel at the Drosophila nerve terminal. Furthermore, the slowpoke mutation suppresses the striking increase in transmitter release that occurs following application of 4-aminopyridine to the ether a go-go mutant. This suppression is most likely the result of a reduction of Ca2+ influx into the nerve terminal in the slowpoke mutant. We hypothesize that the effects of the slowpoke mutation are indirect, perhaps resulting from increased Ca2+ channel inactivation, decreased Na+ or Ca2+ channel localization or gene expression, or by increases in the expression or activity of potassium channels distinct from slowpoke.
钾通道控制神经末梢的复极化，因此在突触传递的控制中发挥重要作用。在此，我们描述了慢poke基因（一种钙激活钾通道的结构基因）的突变对黑腹果蝇神经肌肉接头处递质释放的影响。令人惊讶的是，我们发现与正常情况相比，慢poke突变体的递质释放减少。同样，慢poke突变显著抑制了由Shaker突变或应用4-氨基吡啶（它在果蝇神经末梢阻断Shaker编码的钾通道）所导致的递质释放增加。此外，慢poke突变抑制了将4-氨基吡啶应用于ether a go-go突变体后出现的递质释放显著增加。这种抑制很可能是慢poke突变体中进入神经末梢的Ca2+内流减少的结果。我们推测慢poke突变的影响是间接的，可能是由于Ca2+通道失活增加、Na+或Ca2+通道定位或基因表达减少，或者是由于不同于慢poke的钾通道的表达或活性增加所致。
