SLO-1 potassium channels control quantal content of neurotransmitter release at the C. elegans neuromuscular junction

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.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Amino Acid Sequence
  • Animals
  • Caenorhabditis elegans / genetics
  • Caenorhabditis elegans / metabolism
  • Caenorhabditis elegans Proteins
  • Excitatory Postsynaptic Potentials / physiology
  • Large-Conductance Calcium-Activated Potassium Channels
  • Molecular Sequence Data
  • Mutation / genetics
  • Neuromuscular Junction / genetics
  • Neuromuscular Junction / metabolism*
  • Neurotransmitter Agents / genetics
  • Neurotransmitter Agents / metabolism*
  • Potassium Channels / physiology*
  • Potassium Channels, Calcium-Activated / genetics
  • Potassium Channels, Calcium-Activated / metabolism
  • Potassium Channels, Calcium-Activated / physiology*
  • Presynaptic Terminals / metabolism
  • Xenopus


  • Caenorhabditis elegans Proteins
  • Large-Conductance Calcium-Activated Potassium Channels
  • Neurotransmitter Agents
  • Potassium Channels
  • Potassium Channels, Calcium-Activated
  • slo-1 protein, C elegans

Associated data

  • GENBANK/AF431891
  • GENBANK/AF431892
  • GENBANK/AF431893