A group of neurons in the nucleus of the solitary tract (NTS) contains the mineralocorticoid receptor (MR) which makes these neurons candidates for stimulating salt intake in response to aldosterone. The purpose of this study was to determine if neurons within the NTS that possess the MR play a role in aldosterone stimulation of salt intake. Five adult WKY rats received microinjections into the NTS of a small, hairpin RNA (shRNA) for the MR (Genedetect, Inc.) and 5 rats received NTS injections of a scrambled RNA (scRNA). In each rat injections of viral constructs were made at 3 points, all 0.5mm below the surface of the brain: calamus; bilaterally at 0.5mm rostral to calamus and 0.5mm lateral to the midline. One week after the viral construct injections, aldosterone-filled osmotic mini-pumps were implanted subcutaneously and connected to tubing within the 4 th ventricle to infuse aldosterone at a rate of 20ng/h. Prior to and after surgeries, rats had ad libitum access to food and two graduated drinking bottles filled with distilled water and 0.3M NaCl respectively. Fluid level within each bottle was measured at the same time every day and salt intake expressed as 100 X the ratio of 0.3M NaCl intake to total fluid intake. Previous studies indicate that the viral constructs require 2 weeks to have a discernible effect. One week after injection of the viral constructs and prior to infusion of implantation of the aldosterone mini-pump, salt intake in shRNA injected rats was 6% ± 3% and in scRNA injected rats it was 4% ± 2%. One week after beginning aldosterone infusion (two weeks after injection of viral constructs), salt intake in shRNA injected rats was 16% ± 5% and in scRNA injected rats it was 22% ± 7% (p=0.01). Three weeks after beginning aldosterone infusion, salt intake in shRNA injected rats was 5% ± 2% and in scRNA injected rats it was 14% ± 9% (p=0.01). Post-mortem immunohistochemistry revealed a significant reduction in the number of NTS neurons exhibiting immunoreactivity for the MR (shRNA 2 ± 2 cells/section; scRNA 12 ± 2 cells/section; p=.008). These results indicate hindbrain infusions of aldosterone stimulate salt intake and that at least part of the hindbrain aldosterone stimulation of salt intake are mediated by hindbrain NTS neurons that possess the MR.