RESUMO
In the present paper, we have evaluated the participation of 5-HT(3) and 5-HT(2C) 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(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(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(2C) receptors located in the central amygdala by the selective 5-HT(2C) receptor agonist m-CPP failed to modify salt intake in sodium-depleted rats. Additionally, the administration of a selective 5-HT(2C) 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(3) receptors located within the CeA inhibits salt intake in sodium-depleted rats and that 5-HT(2C) receptors located within the CeA appear to be dissociated from the salt intake control mechanisms operating in the central amygdala.