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

Nature communications | 2014

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 Ca(2+) entry through EGL-19, an L-type voltage-gated Ca(2+) channel (CaV1), but not on other proteins implicated in either Ca(2+) entry or intracellular Ca(2+) release. Thus, SLO-2 is functionally coupled with CaV1 and regulates neurotransmitter release.

Pubmed ID: 25300429 RIS Download

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Associated grants

  • Agency: NIMH NIH HHS, United States
    Id: R01 MH085927
  • Agency: NIMH NIH HHS, United States
    Id: 1R01MH085927

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