Evaluation of the role played by neurosteroids in the ADH-releasing mechanism mediated by forebrain receptors for amino-acid transmitters

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An increase in plasma osmolality and a decrease in blood volume are primary factors to facilitate ADH secretion. Both stimulus excites hypothalamic ADH-releasing cells by causing inactivation of the GABA(A) receptor in a forebrain region called the anteroventral third ventricle(AV3V). It is well known that the GABA(A) receptor includes a lot of subtypes, among which there exists a subtype whose binding affinity to GABA is highly affected by steroids generated in the brain tissue(neurosteroids, NS). However, topical infusions in the AV3V with NS or an inhibitor for the synthesis of NS affected neither basal ADH release nor stimulated ADH secretion by pharmacological blockade of the GABA(A) receptor, plasma hyperosmolality or blood hypovolemia. These results suggest that AV3V GABA(A) receptors involved in ADH secretion may not be regulated acutely at least by NS.