CaMKI-dependent regulation of sensory gene expression mediates experience-dependent plasticity in the operating range of a thermosensory neuron.
- Yu YV Department of Biology, National Center for Behavioral Genomics Brandeis University Waltham, MA 02454.
- Bell HW Department of Biology, National Center for Behavioral Genomics Brandeis University Waltham, MA 02454.
- Glauser D Department of Biology University of Fribourg Fribourg 1700, Switzerland.
- Van Hooser SD Department of Biology, National Center for Behavioral Genomics Brandeis University Waltham, MA 02454.
- Goodman MB Department of Molecular and Cellular Physiology Stanford University School of Medicine Palo Alto, CA 94305.
- Sengupta P Department of Biology, National Center for Behavioral Genomics Brandeis University Waltham, MA 02454.
- 2014-12-04
Published in:
- Neuron. - 2014
Adaptation, Physiological
Analysis of Variance
Animals
Animals, Genetically Modified
Caenorhabditis elegans
Caenorhabditis elegans Proteins
Calcium
Computer Simulation
Cyclic GMP
Green Fluorescent Proteins
Mitogen-Activated Protein Kinase 1
Models, Neurological
Mutation
Neuronal Plasticity
Psychophysics
Sensory Receptor Cells
Temperature
Thermosensing
Time Factors
English
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.
- Language
-
- English
- Open access status
- bronze
- Identifiers
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- DOI 10.1016/j.neuron.2014.10.046
- PMID 25467978
- Persistent URL
- https://sonar.ch/global/documents/138858
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