The amygdala: Site of genomic and nongenomic arousal of aldosterone-induced sodium intake

Background. Mineralocorticoids act on the brain to influence sodium intake, and they do so via intracellular type I receptors and possibly also via a direct membrane action, as they do in the kidney. One brain area implicated by lesion studies investigating the regulation of sodium appetite aroused by adrenal steroids is the amygdala. Methods. To examine the mechanism by which mineralocorticoids act in the am ygdala to arouse salt intake via a genomic and or membrane mode of action, rats were bilaterally fitted with cannulae directed to terminate in the amy gdala. The genomic action of mineralocorticoids in arousing sodium intake w as investigated by the administration of antisense oligodeoxynucleotides (A SDNs) against the mineralocorticoid receptor, and its effects on deoxycorti costerone (DOCA)-induced sodium intake over the course of several days was examined. The nongenomic action of mineralocorticoids on sodium intake was investigated by implantation into the amygdala of DOCA, aldosterone (ALDO), or their A-ring-reduced tetrahydro derivatives, 15 minutes prior to access to saline. Sodium intake was monitored immediately thereafter. Results. Treatment of rats in the amygdala with ASDN against the mineraloco rticoid receptor inhibited DOCA-induced sodium intake, whereas ASDN against the glucocorticoid receptor or sense/scrambled sequences had no effect. DO CA and ALDO increased saline intake within 15 minutes after steroid applica tion. Similarly, the application of A-ring-reduced 3 beta,5 beta tetrahydro aldosterone and 5 alpha-tetrahydrodeoxycorticosterone produced the same inc reases in sodium intake. Conclusions. Together, the data imply that adrenal steroids, in addition to acting through classic cytosolic receptors, may also act on membrane recep tor systems, producing rapid changes in behavior.