TRPV1 and Osmoregulation

Central control of systemic osmoregulation is the job of the organum vasculosum lamina terminalis (OVLT), located at the rostral ventral edge of the third ventricle. In this week’s Journal, Ciura and Bourque demonstrate that OVLT neurons are intrinsically osmosensitive because they express transient receptor potential vanilloid 1 (TRPV1) channels. The authors compared the neuronal activity of hypothalamic explants from wild-type and TRPV1-deficient mice. OVLT neurons in wild-type mice responded to increased osmolality with an increased firing rate, whereas TRPV1 / neurons did not. OVLT neurons responded directly to the change in osmolality with membrane depolarization. Ruthenium red, a blocker of nonselective cation channels, prevented hypertonic solution-induced depolarization, pointing to TRPV1 as the transducer. In vivo, TRPV1 / mice drank less water after an osmotic challenge than did their WT counterparts, placing TRPV1 in the pathway that triggers thirst.