Abstract
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.
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