Journal
CELL REPORTS
Volume 23, Issue 8, Pages 2245-2253Publisher
CELL PRESS
DOI: 10.1016/j.celrep.2018.04.090
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Funding
- Distinguished James McGill Research Chair grant
- Canadian Institutes of Health Research Foundation grant [FDN-143337]
- Heart and Stroke Foundation of Canada [G-16-00014197]
- Canada Graduate Scholarship Award
- AFM-Telethon Trampoline Grant [21488]
- Le Fonds de Recherche du Quebec - Sante
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The maintenance of hydromineral homeostasis requires bidirectional detection of changes in extracellular fluid osmolality by primary osmosensory neurons (ONs) in the organum vasculosum laminae terminalis (OVLT). Hypertonicity excites ONs in part through the mechanical activation of a variant transient receptor potential vanilloid-1 channel (dn-Trpv1). However, the mechanism by which local hypotonicity inhibits ONs in the OVLT remains unknown. Here, we show that hypotonicity can reduce the basal activity of dn-Trpv1 channels and hyperpolarize acutely isolated ONs. Surprisingly, we found that mice lacking dn-Trpv1 maintain normal inhibitory responses to hypotonicity when tested in situ. In the intact setting, hypotonicity inhibits ONs through a non-cell-autonomous mechanism that involves glial release of the glycine receptor agonist taurine through hypotonicity activated anion channels (HAAC) that are activated subsequent to Ca2+ influx through Trpv4 channels. Our study clarifies how Trpv4 channels contribute to the inhibition of OVLT ONs during hypotonicity in situ.
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