SLO-2 potassium channel is an important regulator of neurotransmitter release in Caenorhabditis elegans

Ping Liu, Bojun Chen and Zhao-Wen Wang ()
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Ping Liu: University of Connecticut Health Center
Bojun Chen: University of Connecticut Health Center
Zhao-Wen Wang: University of Connecticut Health Center

Nature Communications, 2014, vol. 5, issue 1, 1-12

Abstract: Abstract Slo2 channels are prominent K+ channels in mammalian neurons but their physiological functions are not well understood. Here we investigate physiological functions and regulation of the Caenorhabditis elegans homologue SLO-2 in motor neurons through electrophysiological analyses of wild-type and mutant worms. We find that SLO-2 is the primary K+ channel conducting delayed outward current in cholinergic motor neurons, and one of two K+ channels with this function in GABAergic motor neurons. Loss-of-function mutation of slo-2 increases the duration and charge transfer rate of spontaneous postsynaptic current bursts at the neuromuscular junction, which are physiological signals used by motor neurons to control muscle cells, without altering postsynaptic receptor sensitivity. SLO-2 activity in motor neurons depends on Ca2+ entry through EGL-19, an L-type voltage-gated Ca2+ channel (CaV1), but not on other proteins implicated in either Ca2+ entry or intracellular Ca2+ release. Thus, SLO-2 is functionally coupled with CaV1 and regulates neurotransmitter release.

Date: 2014
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DOI: 10.1038/ncomms6155

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