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Neuron. 2014 Dec 3;84(5):983-96. doi: 10.1016/j.neuron.2014.10.039. Epub 2014 Nov 20.

The balance between cytoplasmic and nuclear CaM kinase-1 signaling controls the operating range of noxious heat avoidance.

Author information

  • 1Department of Biology, University of Fribourg, 1700 Fribourg, Switzerland.
  • 2Department of Biology and National Center for Behavioral Genomics, Brandeis University, Waltham, MA 02454, USA.
  • 3Department of Molecular and Cellular Physiology, Stanford School of Medicine, Stanford, CA 94305, USA. Electronic address: mbgoodman@stanford.edu.
  • 4Department of Biology, University of Fribourg, 1700 Fribourg, Switzerland. Electronic address: dominique.glauser@unifr.ch.

Abstract

Through encounters with predators, competitors, and noxious stimuli, animals have evolved defensive responses that minimize injury and are essential for survival. Physiological adaptation modulates the stimulus intensities that trigger such nocifensive behaviors, but the molecular networks that define their operating range are largely unknown. Here, we identify a gain-of-function allele of the cmk-1 CaMKI gene in C. elegans and show that loss of the regulatory domain of the CaMKI enzyme produces thermal analgesia and shifts the operating range for nocifensive heat avoidance to higher temperatures. Such analgesia depends on nuclear CMK-1 signaling, while cytoplasmic CMK-1 signaling lowers the threshold for thermal avoidance. CMK-1 acts downstream of heat detection in thermal receptor neurons and controls neuropeptide release. Our results establish CaMKI as a key regulator of the operating range for nocifensive behaviors and suggest strategies for producing thermal analgesia through the regulation of CaMKI-dependent signaling.

PMID:
25467982
PMCID:
PMC4318703
DOI:
10.1016/j.neuron.2014.10.039
[PubMed - indexed for MEDLINE]
Free PMC Article
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