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Acute administration of 5HT1a serotonin receptor agonist, in the dorsal raphe nuclei (DRN) or systemically, increases whereas peripheral chronic treatment inhibits sodium intake in rats

Opposite effects have been attributed to acute or chronic activation of 5HT1a serotonin receptors. In the DRN, somatodendritic 5HT1a receptors are implicated in the auto‐modulation of serotonergic neurons’ activity. We investigated the effects of acute and chronic activation of 5HT1a receptors in spontaneous or induced sodium intake. Agonist (8‐OH‐DPAT, 7.5 nmol) or antagonist (WAY‐100635, 2 nmol) of the 5HT1a receptor was acutely microinjected into the DRN of furosemide sodium‐depleted rats. 8‐OH‐DPAT increased the sodium intake induced by low sodium diet plus depletion by furosemide (20 mg/Kg, sc) (20.1±1.1 vs 24.9±0.9 mL, at 120 min after 0.3M NaCl presentation). WAY‐100635 did not affect sodium intake in the same paradigm. Likewise, a single sc injection of 8‐OH‐DPAT (250 μg/Kg) induced a higher sodium intake (0.03±0.03 mL vs 4.5±0.5 mL, 120 min after 0.3M NaCl presentation). Conversely, chronic administration of 8‐OH‐DPAT (500 μg/Kg/day, ip, during 3 weeks) inhibited induced sodium intake (8.6±0.9 mL vs 5.8±0.4 mL, 60 min after 0.3M NaCl presentation). Water intake was not affected by the treatment. These data suggest that the time course of the 5HT1a activation may differentially affect sodium intake behaviour. It implies a 5HT1a “down‐regulation” or “desensitization” after chronic administration of the agonist. This work was supported by FAPESP # 03/00327‐8; CNPq # 478981/2004‐0, and Capes.