Functional brainstem pathways linked to sodium deprivation and salt intake

Abstract

To reveal brainstem pathways activated by sodium deprivation and salt ingestion, nuclear c-Fos immunoreactivity (a marker for neuronal activity) was examined in neurons within the nucleus of the solitary tract (NTS) and in their efferent target nuclei within the pontine parabrachial complex (PB) in rats. After 8d dietary sodium deprivation, the aldosterone-sensitive neurons in the NTS, which express 11-β-hydroxysteroid dehydrogenase type 2 (HSD2), exhibited a marked increase in c-Fos immunoreactivity. In the PB, c-Fos labeling increased specifically within the two nuclei that relay information from the HSD2 neurons to the forebrain – the pre-locus coeruleus and the inner subdivision of the external lateral nucleus. In separate groups of rats that ingested salt (3% NaCl solution) for 1 or 2h following 8d sodium-deprivation, c-Fos immunoreactivity within the HSD2 neurons was virtually eliminated, whereas a prominent increase in c-Fos labeling was found in the surrounding medial NTS (including A2 noradrenergic neurons) and area postrema. Salt ingestion also increased c-Fos labeling in PB nuclei that relay gustatory (caudal medial PB) and viscerosensory (rostral lateral PB) information from the NTS to the forebrain. Thus, sodium deficiency and salt ingestion stimulate separate subpopulations of neurons within the NTS, which transmit this information to the forebrain via largely separate nuclei in the PB. The existence of parallel, ascending signals for sodium need and salt intake offers a new perspective on the potential functions of brainstem sensory pathways in the regulation of sodium appetite.