Journal
JOURNAL OF NEUROSCIENCE
Volume 33, Issue 43, Pages 17160-17165Publisher
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.1048-13.2013
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Funding
- Canadian Institutes of Health Research [MOP-9939, MOP-82818]
- James McGill Research Chair
- Canada Graduate Scholarships Program
- McGill University
- Fonds de recherche du Quebec-Sante
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The transient receptor potential vanilloid 1 and 4 genes (trpv1, trpv4) encode temperature-sensitive cation channels hypothesized to mediate thermoresponses in mammalian cells. Although such channels were shown to participate in the peripheral detection of ambient temperature, the specific roles of these channels in central thermosensory neurons remain unclear. Here we report that the membrane potential and excitability of mouse magnocellular neurosecretory cells (MNCs) maintained at physiological temperature were lowered in an additive manner upon pharmacological blockade, or genetic deletion, of trpv1 and trpv4. However extracellular recordings from spontaneously active MNCs in situ showed that blockade or genetic deletion of trpv4 does not interfere with thermally induced changes in action potential firing, whereas loss of trpv1 abolished this phenotype. These findings indicate that channels encoded by trpv4 play a permissive role that contributes to basal electrical activity, but that trpv1 plays a dynamic role that is required for physiological thermosensation by MNCs.
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