Caenorhabditis elegans nicotinic acetylcholine receptors are required for nociception

Emiliano Cohen, Marios Chatzigeorgiou, Steven J. Husson, Wagner Steuer-Costa, Alexander Gottschalk, William R. Schafer, Millet Treinin

Research output: Contribution to journalArticlepeer-review


Polymodal nociceptors sense and integrate information on injurious mechanical, thermal, and chemical stimuli. Chemical signals either activate nociceptors or modulate their responses to other stimuli. One chemical known to activate or modulate responses of nociceptors is acetylcholine (ACh). Across evolution nociceptors express subunits of the nicotinic acetylcholine receptor (nAChR) family, a family of ACh-gated ion channels. The roles of ACh and nAChRs in nociceptor function are, however, poorly understood. Caenorhabditis elegans polymodal nociceptors, PVD, express nAChR subunits on their sensory arbor. Here we show that mutations reducing ACh synthesis and mutations in nAChR subunits lead to defects in PVD function and morphology. A likely cause for these defects is a reduction in cytosolic calcium measured in ACh and nAChR mutants. Indeed, overexpression of a calcium pump in PVD mimics defects in PVD function and morphology found in nAChR mutants. Our results demonstrate, for the first time, a central role for nAChRs and ACh in nociceptor function and suggest that calcium permeating via nAChRs facilitates activity of several signaling pathways within this neuron.

Original languageAmerican English
Pages (from-to)85-96
Number of pages12
JournalMolecular and Cellular Neuroscience
StatePublished - Mar 2014


  • Acetylcholine
  • Caenorhabditis elegans
  • Calcium
  • Nicotinic acetylcholine receptors
  • Polymodal nociceptors

All Science Journal Classification (ASJC) codes

  • Molecular Biology
  • Cellular and Molecular Neuroscience
  • Cell Biology


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