Mammals have evolved sophisticated behavioral and physiological respon
ses 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 ar
e controlled by ''osmoreceptors'': groups of specialized nerve cells c
apable of transducing changes in external osmotic pressure into meanin
gful electrical signals. Some of these sensors are located in the regi
on of the hepatic portal vein, a strategic site allowing early detecti
on of the osmotic impact of ingested foods and fluids. Changes in syst
emic osmolality, however, are detected centrally, within regions that
include the medial preoptic area, the median preoptic nucleus, the org
anum vasculosum lamina terminalis (OVLT), the subfornical organ, and t
he supraoptic nucleus (SON). While studies have indicated that these c
entral and peripheral osmoreceptors participate in the control of osmo
regulatory responses, little is known of the mechanisms by which this
is achieved. One notable exception, however, consists of the osmotic c
ontrol of electrical activity in SON neurons which, in the rat, contri
butes to the regulation of natriuresis and diuresis through effects on
the secretion of oxytocin and vasopressin. Previous studies have show
n that these cells are respectively excited and inhibited by hypertoni
c and hypotonic conditions. Experiments in vitro indicate that these r
esponses result from both the endogenous osmosensitivity of these cell
s and changes in synaptic drive. Patch-clamp analysis has revealed tha
t SON neurons are respectively depolarized and hyperpolarized by incre
ases and decreases in external osmolality and that these intrinsic res
ponses result from changes in the activity of mechanosensitive cationi
c channels. Moreover, intracellular recordings in hypothalamic explant
s have shown that changes in electrical activity are associated with p
roportional changes in the frequency of glutamatergic excitatory posts
ynaptic potentials derived from osmosensitive OVLT neurons. Both of th
ese mechanisms, therefore, may participate in the osmotic regulation o
f neurohypophysial hormone release in situ. (C) 1994 Academic Press, I
nc.