Sodium appetite and Fos activation in serotonergic neurons

Abstract

2000.-We evaluated serotonergic hindbrain groups of cells for their involvement in the generation and inhibition of sodium appetite. For that purpose, we analyzed the number of Fos-immunoreactive (Fos-ir) cells and double-labeled Fosserotonin (5-HT)-ir neurons within different nuclei of the hindbrain raphe system and the area postrema (AP). Sodium depletion and sodium appetite were induced by peritoneal dialysis. Twenty-four hours after peritoneal dialysis, a 2% NaCl solution intake test was given to peritoneal dialyzed animals [PD-with access (PD-A) group] and to control dialyzed animals [CD-with access (CD-A) group]. Two additional groups of animals received either peritoneal dialysis or control dialysis but were not given access to the 2% NaCl [CD-no access (CD-NA) group or PD-no access (PD-NA) group]. The number of Fos-ir neurons within different nuclei of the raphe system was increased in spontaneous and induced sodium ingestion of CD-A and PD-A groups compared with the CD-NA and PD-NA groups. The PD-NA group had significantly fewer double-labeled cells along the raphe system compared with the animals in near-normal sodium balance (CD-NA and CD-A) or in the process of restoring sodium balance by consuming NaCl (PD-A). The AP of the PD-A group showed a significant increase in the number of Fos-ir and Fos-5-HT-ir cells compared with the PD-NA and CD groups. Our results suggest that serotonergic pathways with cell bodies in the AP and the raphe system are involved in the control of sodium appetite.Fos-serotonin immunoreactivity; area postrema; raphe system RECENTLY, there has been increased interest in identifying the neural network subserving sodium appetite. Forebrain structures such us the circumventricular organs (CVOs) of the lamina terminalis, the organum vasculosum of the lamina terminalis, and the subfornical organ have been identified as key targets processing angiotensin-, osmotic-, and sodium-related information involved in the control of sodium appetite.A hindbrain system has also been recently implicated in the inhibitory control of sodium appetite. This system includes the neural circuitry of the area postrema (AP), nucleus of the solitary tract (NTS), and lateral parabrachial nucleus (LPBN). Ablation of the AP and the immediately adjacent medial NTS (mNTS) increases induced and ad libitum sodium intake (7, 9, 16). Electrolytic or chemical lesions of the LPBN, which receives afferent projections from the AP/mNTS, also enhance drinking induced by intracerebroventricular ANG II as well as other ANG II-related stimuli (10,28,29). Several studies suggest that a serotonergic hindbrain circuit including the LPBN may normally exert an inhibitory action on several models of reninangiotensin-dependent sodium and water intake (6,22,23; see Ref. 18 for review). In addition, previous evidence has indicated that there are central serotonergic influences on sodium and water intake and excretion (24,27,34,37).Serotonergic neurons are located within several nuclei in the midbrain and the brain stem and have dif...

Chronic excitotoxic lesion of the dorsal raphe nucleus induces sodium appetite

“…Furosemide-induced sodium and water depletion enhanced the natriorexigenic response of IBO-DRN, which became significantly higher than that of PB-DRN only after 240 min of fluid offer, remaining at this level been shared by other investigators who have shown increased c-Fos expression in DRN serotonergic neurons after salt intake under both basal and sodium depletion conditions (11).…”

“…Corroborating these findings, other investigators showed that basal c-Fos expression in serotonergic neurons of the DRN decreased after sodium depletion induced by peritoneal dialysis and increased after spontaneous and induced sodium intake, suggesting that there is a tonic inhibition of sodium appetite by serotonergic cells of this nucleus (11). Although we hypothesized the same, when working with DRN electrolytic lesion it is necessary to limit the lesion to the neuronal cell body located in the ventromedial portion of the DRN and to perform longer observations (21).…”

Effect of electrolytic lesion of the dorsal raphe nucleus on water intake and sodium appetite

“…The SFO and OVLT constitute convergent sites for signals related to volume depletion (4,18,28,29). As mentioned previously, these structures are innervated by serotonergic neurons, are rich in serotonin receptors and reciprocally transmit signals to the raphe (1,2,4-6,8).…”

“…Recent evidence has shown that sodium depletion induced by the combination of furosemide with a low dose of captopril causes an increase in c-Fos expression in the nucleus tractus solitarii (NTS), which is suppressed by renal deafferentation (31). Following the same line of reasoning, evoked potentials were recorded in serotonergic neurons of the DRN after the isoosmotic loss of volume by hemorrhage and, more specifically, induction of c-Fos expression was determined in serotonergic neurons of the DRN and in structures of the lamina terminalis after sodium depletion by peritoneal dialysis (7,18).…”

“…The authors reported an inhibition of water intake after dipsogenic challenges induced by fluid deprivation, hypertonic saline overload or hypovolemia. Furthermore, it has been shown that basal c-Fos expression in serotoninergic neurons of the DRN was decreased after sodium depletion induced by peritoneal dialysis and was increased after spontaneous and induced sodium intake, suggesting that there is a tonic inhibition of sodium appetite by serotoninergic cells of this nucleus (18).…”