Osmoreceptors, osmoreception, and osmoregulation

C.W. Bourque, S.H.R. Oliet, D. Richard
Frontiers in Neuroendocrinology. 1994-09-01; 15(3): 231-274
DOI: 10.1006/frne.1994.1010

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1. Front Neuroendocrinol. 1994 Sep;15(3):231-74.

Osmoreceptors, osmoreception, and osmoregulation.

Bourque CW(1), Oliet SH, Richard D.

Author information:
(1)Centre for Research in Neuroscience, Montreal General Hospital, P.Q., Canada.

Mammals have evolved sophisticated behavioral and physiological responses to
oppose changes in the osmolality of their extracellular fluid. The behavioral
approach consists of regulating the intake of salt and water through changes in
sodium appetite and thirst. The physiological approach comprises adjustments of
renal excretion of water and sodium which are achieved through changes in the
release of antidiuretic and natriuretic hormones. Individually, these
osmoregulatory responses are controlled by “osmoreceptors”: groups of specialized
nerve cells capable of transducing changes in external osmotic pressure into
meaningful electrical signals. Some of these sensors are located in the region of
the hepatic portal vein, a strategic site allowing early detection of the osmotic
impact of ingested foods and fluids. Changes in systemic osmolality, however, are
detected centrally, within regions that include the medial preoptic area, the
median preoptic nucleus, the organum vasculosum lamina terminalis (OVLT), the
subfornical organ, and the supraoptic nucleus (SON). While studies have indicated
that these central and peripheral osmoreceptors participate in the control of
osmoregulatory responses, little is known of the mechanisms by which this is
achieved. One notable exception, however, consists of the osmotic control of
electrical activity in SON neurons which, in the rat, contributes to the
regulation of natriuresis and diuresis through effects on the secretion of
oxytocin and vasopressin. Previous studies have shown that these cells are
respectively excited and inhibited by hypertonic and hypotonic conditions.
Experiments in vitro indicate that these responses result from both the
endogenous osmosensitivity of these cells and changes in synaptic drive.
Patch-clamp analysis has revealed that SON neurons are respectively depolarized
and hyperpolarized by increases and decreases in external osmolality and that
these intrinsic responses result from changes in the activity of mechanosensitive
cationic channels. Moreover, intracellular recordings in hypothalamic explants
have shown that changes in electrical activity are associated with proportional
changes in the frequency of glutamatergic excitatory postsynaptic potentials
derived from osmosensitive OVLT neurons. Both of these mechanisms, therefore, may
participate in the osmotic regulation of neurohypophysial hormone release in

DOI: 10.1006/frne.1994.1010
PMID: 7859914 [Indexed for MEDLINE]

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