Send to

Choose Destination
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

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


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.

[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for PubMed Central
Loading ...
Support Center