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Neuron. 2014 Dec 3;84(5):919-926. doi: 10.1016/j.neuron.2014.10.046. Epub 2014 Nov 20.

CaMKI-dependent regulation of sensory gene expression mediates experience-dependent plasticity in the operating range of a thermosensory neuron.

Author information

1
Department of Biology, National Center for Behavioral Genomics Brandeis University Waltham, MA 02454.
2
Department of Biology University of Fribourg Fribourg 1700, Switzerland.
3
Department of Molecular and Cellular Physiology Stanford University School of Medicine Palo Alto, CA 94305.
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Contributed equally

Abstract

Sensory adaptation represents a form of experience-dependent plasticity that allows neurons to retain high sensitivity over a broad dynamic range. The mechanisms by which sensory neuron responses are altered on different timescales during adaptation are unclear. The threshold for temperature-evoked activity in the AFD thermosensory neurons (T*(AFD)) in C. elegans is set by the cultivation temperature (T(c)) and regulated by intracellular cGMP levels. We find that T*(AFD) adapts on both short and long timescales upon exposure to temperatures warmer than T(c), and that prolonged exposure to warmer temperatures alters expression of AFD-specific receptor guanylyl cyclase genes. These temperature-regulated changes in gene expression are mediated by the CMK-1 CaMKI enzyme, which exhibits T(c)-dependent nucleocytoplasmic shuttling in AFD. Our results indicate that CaMKI-mediated changes in sensory gene expression contribute to long-term adaptation of T*(AFD), and suggest that similar temporally and mechanistically distinct phases may regulate the operating ranges of other sensory neurons.

PMID:
25467978
PMCID:
PMC4258139
DOI:
10.1016/j.neuron.2014.10.046
[Indexed for MEDLINE]
Free PMC Article

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