Wang Z W, Saifee O, Nonet M L, Salkoff L
Department of Anatomy and Neurobiology, Washington University School of Medicine, Campus Box 8108, 660 S. Euclid Avenue, St. Louis, MO 63110, USA.
Neuron. 2001 Dec 6;32(5):867-81. doi: 10.1016/s0896-6273(01)00522-0.
Six mutants of SLO-1, a large-conductance, Ca(2+)-activated K(+) channel of C. elegans, were obtained in a genetic screen for regulators of neurotransmitter release. Mutants were isolated by their ability to suppress lethargy of an unc-64 syntaxin mutant that restricts neurotransmitter release. We measured evoked postsynaptic currents at the neuromuscular junction in both wild-type and mutants and observed that the removal of SLO-1 greatly increased quantal content primarily by increasing duration of release. The selective isolation of slo-1 as the only ion channel mutant derived from a whole genomic screen to detect regulators of neurotransmitter release suggests that SLO-1 plays an important, if not unique, role in regulating neurotransmitter release.
在一项针对神经递质释放调节因子的遗传筛选中，获得了秀丽隐杆线虫大电导钙激活钾通道SLO-1的六个突变体。这些突变体是通过其抑制unc-64突触融合蛋白突变体（该突变体限制神经递质释放）引起的嗜睡能力而分离出来的。我们测量了野生型和突变体神经肌肉接头处诱发的突触后电流，发现去除SLO-1主要通过增加释放持续时间，极大地增加了量子含量。从全基因组筛选中选择性分离出slo-1作为唯一检测神经递质释放调节因子的离子通道突变体，这表明SLO-1在调节神经递质释放中发挥着重要作用（即便不是独特作用）。
