Abstract
Ablation of the area postrema/caudal nucleus of the tractus solitarius (NTS) complex increases sodium intake, but the effect of selective lesions of the caudal NTS is not known. We measured depletion-induced sodium intake in rats with electrolytic lesions of the commissural NTS that spared the area postrema. One day after the lesion, rats were depleted of sodium with furosemide (10 mg/kg body weight, sc) and then had access to water and a sodium-deficient diet for 24 h when 1.8% NaCl was offered. Water and saline intakes were measured for 2 h. Saline intake was higher in lesioned than in sham-lesioned rats (mean +/- SEM: 20 +/- 2 vs 11 +/- 3 mL/2 h, P < 0.05, N = 6-7). Saline intake remained elevated in lesioned rats when the tests were repeated 6 and 14 days after the lesion, and water intake in these two tests was increased as well. Water intake seemed to be secondary to saline intake both in lesioned and in sham-lesioned rats. A second group of rats was offered 10% sucrose for 2 h/day before and 2, 7, and 15 days after lesion. Sucrose intake in lesioned rats was higher than in sham-lesioned rats only 7 days after lesioning. A possible explanation for the increased saline intake in rats with commissural NTS lesions could be a reduced gastrointestinal feedback inhibition. The commissural NTS is probably part of a pathway for inhibitory control of sodium intake that also involves the area postrema and the parabrachial nucleus.
Highlights
Sodium depletion stimulates the intake of salty solutions
Sodium depletion stimulates the production of angiotensin II, which acts on the vascular organ of the lamina terminalis and the subfornical organ in the forebrain to stimulate salt intake
Five from 8 lesioned rats were included for data analysis in the sucrose intake group
Summary
Sodium depletion stimulates the intake of salty solutions. The lateral parabrachial nucleus can powerfully inhibit sodium intake [1,2]. Especially the area postrema and the adjacent nucleus of the solitary tract (NTS), affect the intake of sodium, but their function is less clear. This region receives visceral and cardiovascular vagal information, and it has been suggested that lesions in this area affect fluid intake by disrupting feedback inhibition [3]. Neighboring regions may have opposite effects on sodium intake. Area postrema lesions that include parts of the NTS are less effective in stimulating saline intake than area postrema lesions that leave the NTS intact [6]
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