Mechanosensitive channels transduce osmosensitivity in supraoptic neurons.
Nature. 1993-07-01; 364(6435): 341-343
DOI: 10.1038/364341a0
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Vasopressin is a peptide hormone synthesized by neurons of the supraoptic and
paraventricular nuclei, which project axon terminals to the neurohypophysis.
Consistent with its antidiuretic properties, vasopressin release rises as a
function of plasma osmolality, a response that results from accelerated action
potential discharge. Previous studies have shown that increases in fluid
osmolality depolarize supraoptic neurons in the absence of synaptic transmission,
suggesting that these cells behave as intrinsic osmoreceptors. The mechanism by
which changes in osmolality are transduced into an electrical signal is unknown,
however. Here we report that changes in cell volume accompany physiological
variations in fluid osmolality and that these modulate the activity of
mechanosensitive cation channels in a way that is consistent with the macroscopic
regulation of membrane voltage and action potential discharge. These findings
define a function for stretch-inactivated channels in mammalian central neurons.