Sensors for antidiuresis and thirst—osmoreceptors or CSF sodium detectors?

McKinley, MJ; Denton, Derek A.; Weisinger, R. S.

doi:10.1016/0006-8993(78)90619-4

Cited by 245 publications

(127 citation statements)

References 35 publications

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“…Studies combining systemic infusions, intracerebroventricular injection, and fluid sampling, along with neuroendocrine and behavioral analysis, subsequently established that an increase in the osmotic pressure of the CSF is sufficient to induce thirst and vasopressin release in unanesthetized animals (Andersson, 1971;McKinley et al, 1978;Buggy et al, 1979;Thrasher et al, 1980). Lesion studies performed in vivo and in vitro ultimately localized the primary homeostatic osmosensory area to the OVLT, a small circumventricular organ that borders the dorsal aspect of the preoptic recess of the third ventricle (McKinley et al, 1982;Thrasher et al, 1982;Sladek and Johnson, 1983).…”

Section: Discussionmentioning

confidence: 99%

Transient Receptor Potential Vanilloid 1 Is Required for Intrinsic Osmoreception in Organum Vasculosum Lamina Terminalis Neurons and for Normal Thirst Responses to Systemic Hyperosmolality

Ciura¹,

Bourque²

2006

J. Neurosci.

242

255

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Recent studies have indicated that members of the transient receptor potential vanilloid (TRPV) family of cation channels are required for the generation of normal osmoregulatory responses, yet the mechanism of osmosensory transduction in primary osmoreceptor neurons of the CNS remains to be defined. Indeed, despite ample evidence suggesting that the organum vasculosum lamina terminalis (OVLT) serves as the primary locus of the brain for the detection of osmotic stimuli, evidence that neurons in the OVLT are intrinsically osmosensitive has remained elusive. Here we show that murine OVLT neurons are intrinsically sensitive to increases in the osmolality of the extracellular fluid. Hypertonic conditions provoked increases in membrane cation conductance that resulted in the generation of an inward current, depolarizing osmoreceptor potentials, and enhanced action potential discharge. Moreover, we found that this osmosensory signal transduction cascade was absent in OVLT neurons from TRPV1 knock-out (TRPV1 Ϫ/Ϫ ) mice and that responses of wild type (WT) OVLT neurons could be blocked by ruthenium red, an inhibitor of TRPV channels. Finally, TRPV1 Ϫ/Ϫ mice showed significantly attenuated water intake in response to systemic hypertonicity compared with WT controls. These findings indicate that OVLT neurons act as primary osmoreceptors and that a product of the trpv1 gene is required for osmosensory transduction.

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Section: Discussionmentioning

confidence: 99%

Transient Receptor Potential Vanilloid 1 Is Required for Intrinsic Osmoreception in Organum Vasculosum Lamina Terminalis Neurons and for Normal Thirst Responses to Systemic Hyperosmolality

Ciura¹,

Bourque²

2006

J. Neurosci.

242

255

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“…However, the findings in more recent studies seem to contradict the Na receptor concept; the organ-cultured explant of the rat hypothalamo-neurohypophyseal system releases vasopressin in response to an increase in osmolality of the culture medium due to the addition of mannitol as well as NaCI (SLADEK and KNIGGE, 1977). Intraventricular infusion of artificial CSF made hypertonic by the addition of either NaCI or sucrose cause vasopressin release in dogs (THRASHER et al, 1980a), and antidiuresis in sheep (MCKINLEY et al, 1978), although hypertonic NaCI CSF produced a greater antidiuretic effect than hypertonic sucrose.CSF (MCKINLEY et al, 1978). There has been no direct evidence that osmoreceptors rather than Na receptors play a role in the control of oxytocin release except an electrophysiological finding that identified AND OXYTOCIN RELEASE 29 oxytocin cells were excited by i.p.…”

Section: Discussionmentioning

confidence: 99%

“…But this does not seem to be a phenomenon unique to oxytocin release. MCKINLEY et al (1978) who investigated the effect of the infusion of various hypertonic solutions on free water clearance in conscious sheep also observed that 4.6 or 2 M urea caused a reduction in free water clearance, although the change occurred more slowly than when hyperosmotic NaCI or sucrose was infused. They attributed this phenomenon to the presence of sensor elements situated in brain regions which possess a blood-brain barrier to urea.…”

Section: Discussionmentioning

confidence: 99%

Osmoreceptor mechanism for oxytocin release in the rat.

et al. 1988

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In order to determine whether oxytocin release is controlled by an osmoreceptor mechanism identical with that for vasopressin release, the plasma oxytocin concentration and plasma osmolality were measured during intraatrial infusion and after intraventricular injection of various osmotic solutions in unanesthetized rats. Intraatrial infusion of 0.6 M NaCI Locke solution (LS.) or 1.2 M mannitol L.S. elevated plasma oxytocin significantly, while 1.2 M urea L.S. caused only a small increase and isotonic L.S. did not change in plasma oxytocin. All hypertonic solutions produced significant and similar increases in the plasma osmolality. Plasma oxytocin was positively correlated with plasma osmolality in the animals infused with hypertonic NaCI or mannitol but not in the animals infused with hypertonic urea. The injection of 2 tl of 0.6 M NaCI artificial cerebrospinal fluid (CSF) or 1.2 M mannitol CSF into the third ventricle caused a significant increase in plasma oxytocin immediately (5 min after injection) without changing plasma osmolality, while the intraventricular injection of 1.2 M urea CSF or isotonic CSF produced no significant change in plasma oxytocin. These results indicate that oxytocin release is controlled by osmoreceptors rather than Na receptors, that the adequate stimulus for the osmoreceptors is one which produces cellular dehydration and that the osmoreceptors are located in the brain region which is accessible to osmotic agents from both the outside and inside of the bloodbrain barrier. Since the organum vasculosum of the lamina terminalis (OVLT) lacks a blood-brain barrier and is known to be involved in osmotic control of vasopressin release, a lesion was made in the anteroventral region of the third ventricle which encompasses the OVLT and the effect of hypertonic NaCI infusion on oxytocin release was examined. No significant increase in plasma oxytocin was observed after intraatrial infusion of 0.6 M NaCI L.S. in the lesioned rats. All of these findings lead to the conclusion that oxytocin release is under the control of osomoreceptors identical to those for vasopressin release.

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“…Early physiological studies suggested that the mammalian brain detects systemic hypertonicity through a process involving cellular dehydration because hyperosmolality induced by the addition of membrane permeant solutes that do not cause shrinking (e.g., urea) failed to elicit osmoregulatory responses (Gilman, 1937;Verney, 1947;McKinley et al, 1978;Ramsay et al, 1983). Although these findings indicated that extraction of cellular water is a requirement for hypertonicity sensing, they did not reveal whether this process specifically requires shrinking or a concentration of solutes in the cytoplasm.…”

Section: Hypertonicity Sensing Is a Mechanical Processmentioning

confidence: 99%

Hypertonicity Sensing in Organum Vasculosum Lamina Terminalis Neurons: A Mechanical Process InvolvingTRPV1But NotTRPV4

Ciura¹,

Liedtke²,

Bourque³

2011

J. Neurosci.

117

102

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. At present, the mechanism by which hypertonicity modulates cation channels in OVLT neurons is unknown, and it remains unclear whether Trpv1 and Trpv4 both contribute to this process. Here, we show that physical shrinking is necessary and sufficient to mediate hypertonicity sensing in OVLT neurons isolated from adult mice. Steps coupling progressive decreases in cell volume to increased neuronal activity were quantitatively equivalent whether shrinking was evoked by osmotic pressure or mechanical aspiration. Finally, modulation of OVLT neurons by tonicity or mechanical stimulation was unaffected by deletion of trpv4 but was abolished in cells lacking Trpv1 or wild-type neurons treated with the TRPV1 antagonist SB366791. Thus, hypertonicity sensing is a mechanical process requiring Trpv1, but not Trpv4.

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Sensors for antidiuresis and thirst—osmoreceptors or CSF sodium detectors?

Cited by 245 publications

References 35 publications

Transient Receptor Potential Vanilloid 1 Is Required for Intrinsic Osmoreception in Organum Vasculosum Lamina Terminalis Neurons and for Normal Thirst Responses to Systemic Hyperosmolality

Transient Receptor Potential Vanilloid 1 Is Required for Intrinsic Osmoreception in Organum Vasculosum Lamina Terminalis Neurons and for Normal Thirst Responses to Systemic Hyperosmolality

Osmoreceptor mechanism for oxytocin release in the rat.

Hypertonicity Sensing in Organum Vasculosum Lamina Terminalis Neurons: A Mechanical Process InvolvingTRPV1But NotTRPV4

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