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This Article Full Text Full Text (PDF) All Versions of this Article: 92/3/499    most recent expphysiol.2006.035634v1 Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Bourque, C. W. Articles by Sharif-Naeini, R. Search for Related Content PubMed PubMed Citation Articles by Bourque, C. W. Articles by Sharif-Naeini, R. Related Collections Symposia Papers

¹ Centre for Research in Neuroscience, Montreal General Hospital and McGill University, 1650 Cedar Avenue, Montreal QC, Canada H3G 1A4

Abstract

In mammals, the osmolality of the extracellular fluid is maintained near a predetermined set-point through a negative feedback regulation of thirst, diuresis, salt appetite and natriuresis. This homeostatic control is believed to be mediated by osmosensory neurones which synaptically regulate the electrical activity of command neurones that mediate each of these osmoregulatory effector responses. Our present understanding of the molecular, cellular and network basis that underlies the central control of osmoregulation is largely derived from studies on primary osmosensory neurones in the organum vasculosum lamina terminalis (OVLT) and effector neurones in the supraoptic nucleus (SON), which release hormones that regulate diuresis and natriuresis. Primary osmosensory neurones in the OVLT exhibit changes in action potential firing rate that vary in proportion with ECF osmolality. This effect results from 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 neurones then regulate the electrical activity of downstream neurones in the SON through graded changes in glutamate release.

(Received 31 January 2007; accepted after revision 28 February 2007; first published online 9 March 2007)
Corresponding author C. W. Bourque: Centre for Research in Neuroscience, Montreal General Hospital and McGill University, 1650 Cedar Avenue, Montreal QC, Canada H3G 1A4. Email: charles.bourque{at}mcgill.ca

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