Received January 31, 2007
Revised February 20, 2007
Accepted after revision February 28, 2007

¹ Montreal General Hospital & McGill University
² McGill University

^* To whom correspondence should be addressed. E-mail: charles.bourque{at}mcgill.ca.

	Abstract

In mammals, the osmolality of the extracellular fluid is maintained near a pre-determined set-point through a negative feedback regulation of thirst, diuresis, salt appetite and natriuresis. This homeostatic control is believed to be mediated by osmosensory neurons which synaptically regulate the electrical activity of command neurons that mediate each of these osmoregulatory effector responses. Our current understanding of the molecular, cellular, and network basis that underlies the central control of osmoregulation is largely derived from studies on primary osmosensory neurons in the organum vasculosum lamina terminalis (OVLT) and effector neurons in the supraoptic nucleus (SON), which release hormones that regulate diuresis and natriuresis. Primary osmosensory neurons in the OVLT display changes in action potential firing rate that vary in proportion with ECF osmolality. This effect is due to the intrinsic depolarizing receptor potential which these cells generate via a molecular transduction complex that may comprise various members of the transient receptor potential vanilloid (TRPV) family of cation channel proteins, notably TRPV1 and TRPV4. Osmotically-evoked changes in the firing rate of OVLT neurons then regulate the electrical activity of downstream neurons in the SON through graded changes in glutamate release.

Key Words: Hypothalamus, Neurophysiology, Osmoregulation

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