The central amygdala regulates sodium intake in sodium-depleted rats: Role of 5-HT sub(3) and 5-HT sub(2) sub(C) receptors

In the present paper, we have evaluated the participation of 5-HT sub(3) and 5-HT sub(2) sub(C) receptors in the central amygdala (CeA) in the regulation of water and salt intake in sodium-depleted rats. m-CPBG-induced pharmacological activation of 5-HT sub(3) receptors located in the CeA resulted i...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Brain research 2007-03, Vol.1139, p.178-194
Hauptverfasser: Luz, C P, Souza, A, Reis, R, Mineiro, P, Ferreira, H S, Fregoneze, J B, De Castro e Silva, E
Format: Artikel
Sprache:eng
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
Beschreibung
Zusammenfassung:In the present paper, we have evaluated the participation of 5-HT sub(3) and 5-HT sub(2) sub(C) receptors in the central amygdala (CeA) in the regulation of water and salt intake in sodium-depleted rats. m-CPBG-induced pharmacological activation of 5-HT sub(3) receptors located in the CeA resulted in a significant reduction in salt intake in sodium-depleted rats. This antinatriorexic effect of m-CPBG was reverted by pretreatment with the selective 5-HT sub(3) receptor antagonist ondansetron. The injection of ondansetron alone into the CeA had no effect on sodium-depleted and normonatremic rats. Conversely, pharmacological stimulation of 5-HT sub(2) sub(C) receptors located in the central amygdala by the selective 5-HT sub(2) sub(C) receptor agonist m-CPP failed to modify salt intake in sodium-depleted rats. Additionally, the administration of a selective 5-HT sub(2) sub(C) receptor blocker, SDZ SER 082, failed to modify salt intake in rats submitted to sodium depletion. These results lead to the conclusion that the pharmacological activation of 5-HT sub(3) receptors located within the CeA inhibits salt intake in sodium-depleted rats and that 5-HT sub(2) sub(C) receptors located within the CeA appear to be dissociated from the salt intake control mechanisms operating in the central amygdala.
ISSN:0006-8993
DOI:10.1016/j.brainres.2007.01.012