SLO-1 potassium channels control quantal content of neurotransmitter release at the C. elegans neuromuscular junction
SLO-1 potassium channels control quantal content of neurotransmitter release at the C. elegans neuromuscular junction
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DOI：
10.1016/s0896-6273(01)00522-0
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发表时间：
2001-12-06
期刊：
影响因子：
16.2
通讯作者：
Salkoff, L
中科院分区：
文献类型：
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作者：
Wang, ZW;Saifee, O;Salkoff, L
在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的大电导、Ca2+激活的K+通道SLO-1的6个突变体。通过抑制unc-64 syntaxin突变体抑制神经递质释放的能力分离出突变体。我们测量了野生型和突变型神经肌肉连接处诱发的突触后电流，观察到去除SLO-1主要通过增加释放时间大大增加量子含量。从全基因组筛选中选择性分离出唯一的离子通道突变体，以检测神经递质释放的调节因子，这表明，即使不是唯一的，slo-1在调节神经递质释放方面也起着重要的作用。
Six mutants of SLO-1, a large-conductance, Ca2+-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 quanta[ 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.