Role of the serotoninergic system in the sodium appetite control

Abstract

The present article reviews the role of the serotoninergic system in the regulation of the sodium appetite. Data from the peripheral and icv administration of serotoninergic (5-HTergic) agents showed the participation of 5-HT2/3 receptors in the modulation of sodium appetite. These observations were extended with the studies carried out after brain serotonin depletion, lesions of DRN and during blockade of 5-HT2A/2C receptors in lateral parabrachial nucleus (LPBN). Brain serotonin depletion and lesions of DRN increased the sodium appetite response, in basal conditions, after sodium depletion and hypovolemia or after beta-adrenergic stimulation as well. These observations raised the hypothesis that the suppression of ascending pathways from the DRN, possibly, 5-HTergic fi bers, modifi es the angiotensinergic or sodium sensing mechanisms of the subfornical organ involved in the control of the sodium appetite. 5-HTergic blockade in LPBN induced to similar results, particularly those regarded to the natriorexigenic response evoked by volume depletion or increase of the hypertonic saline ingestion induced by brain angiotensinergic stimulation. In conclusion, many evidences lead to acceptation of an integrated participation resulting of an interaction, between DRN and LPBN, for the sodium appetite control.

Mapping brain Fos immunoreactivity in response to water deprivation and partial rehydration: Influence of sodium intake

“…Finally, there was a significant effect of treatment on Fos-ir in CeA [F (3,14 ) = 100.0; p < 0.05]. Fos-ir increased in CeA of WD compared to H group (p < 0.05, Fig.…”

“…Signals from AP, as well as second order neurons in the NTS that sense blood volume through baroreceptors, send projections that reinforce sympathetic activation of the cardiovascular system, and ascend to control thirst as well as vasopressin and oxytocin secretion [8,10]. AP, NTS, DRN, LPBN and CeA, in addition to the lamina terminalis and PVN, belong to overlapping circuits postulated to control neurohypophysial hormone secretion, thirst and sodium appetite [4,[10][11][12][13][14].…”

“…Although these areas play a broader role in body fluid homeostasis, for the purposes of the present study, we have operationally defined them in the context of the control of sodium appetite as either facilitatory or inhibitory, based on previous studies that employed lesions or neurochemical manipulations [8,14]. We consider lamina terminalis and CeA facilitatory to sodium intake, and NTS, LPBN, DRN and AP inhibitory to sodium intake.…”

Role of the lateral parabrachial nucleus in the control of sodium appetite

“…Such inhibition is possibly linked to reduced ANP release and modulation of forebrain activity in circumventricular organs (9,87,109,110). Moreover, in sodium-depleted rats, the ingestion of hypertonic or isotonic saline results in reduced activity in serotonin neurons of the DRN (54, 69).…”

Inhibition of sodium appetite by lipopolysaccharide: involvement of α2-adrenoceptors

“…In addition to the catecholaminergic systems, LPS may also activate the dorsal raphe nucleus serotonergic neurons through a complex transduction mechanism localized in the blood-brain barrier involving immune cells, vascular cells, and cytokines (25). The dorsal raphe nucleus is also involved with serotonergic inhibitory mechanisms of sodium intake (33), and it sends projections to the lateral parabrachial nucleus (LPBN), which apparently is part of the same circuit (8). This raises the possibility that LPS also recruits the putative raphe-LPBN inhibitory system.…”