Integration of sodium and osmosensory signals in vasopressin neurons

Vasopressin (antidiuretic hormone) release has been thought to be controlled by interacting osmoreceptors and Na+-detectors for >20 years. Only recently, however, have molecular and cellular advances revealed how changes in the external concentration of Na+ and osmolality are detected during acute and chronic osmotic perturbations. In rat vasopressin-containing neurons, local osmosensitivity is conferred by intrinsic stretch-inactivated cation channels and by taurine release from surrounding glia. Na+ detection is accomplished by acute regulation of the permeability of stretch-inactivated channels and by changes in Na+ channel gene expression. These features provide a first glimpse of the integrative processes at work in a central osmoregulatory reflex. Recent studies provide cellular and molecular insights on how changes in osmotic pressure and sodium concentration are detected and integrated in central osmoregulatory neurons.