Changes in sodium appetite evoked by lesions of the commissural nucleus of the tractus solitarius

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.

Inhibitory effect of activation of GABAA receptor in the central nucleus of amygdala on the sodium intake in the sodium-depleted rat

“…NS + mus, saline + muscimol. Menani et al, 1998;de Oliveira et al, 2007;David et al, 2008), while lesion of this pathway enhanced sodium and water intake in the sodium-depleted rats induced by acute and chronic sodium depletion (Contreras and Stetson, 1981;Ogihara et al, 2009). Importantly, The CeA not only receives the ascending projection from the brainstem of NTS and PBN, but also contains neurons that descendingly project to the NTS and PBN (Voshart and van der Kooy, 1981;Halsell, 1998;Whitehead et al, 2000;Jia et al, 2005) and modulates the brainstem taste neuronal activity in the ingestion behavior (Li et al, 2002(Li et al, , 2005Kang et al, 2004).…”

Mineralocorticoid receptor in the NTS stimulates saline intake during fourth ventricular infusions of aldosterone

“…Right atrial stretch leads to activation of atrial mechanoreceptors and reduced salt intake, and NTS lesions increase salt intake (8,21). Other studies have shown activation of HSD2 neurons in the NTS during sodium depletion, evidenced by increased immunoreactivity for c-fos (an early gene product of neuronal activation) suggesting a stimulatory role for these neurons during periods of sodium depletion (15).…”

Inhibitory mechanism of the nucleus of the solitary tract involved in the control of cardiovascular, dipsogenic, hormonal, and renal responses to hyperosmolality

“…Therefore, the NTS may be a link between peripheral afferents and brain areas involved in the control of fluid-electrolyte balance and cardiovascular regulation. Accordingly, commissural NTS (commNTS) lesions increased water intake induced by subcutaneous isoproterenol, a stimulus that increases peripheral ANG II (5) or sodium intake induced by sodium depletion (37). Lesions of the commNTS also increased pressor responses dependent on sympathetic/ vasopressinergic activation like those produced by intracerebroventricular injection of noradrenaline or the cholinergic agonist carbachol (55).…”