Papel dos receptores 5-HT1A do núcleo dorsal da rafe no mecanismo de saciedade ao sódio em ratos WISTAR

Abstract

We investigated the possible role of 5-HT1A somatodendritic autoreceptors in the dorsal raphe nucleus (DRN) on salt intake response during basal conditions and following natriorexigenic challenge aroused by sodium depletion in rats. Rats in condiction basal, rats submitted to protocols of sodium depletion, where the animals were treated with furosemide (20mg/kg, SC), protocol FUROCAP, modified FUROCAP, beta-adrenergic stimulated or modified beta-adrenergic protocols rats. Animals that were treated with furosemide were divided into two groups of rats with sodium depletion: one without access to water, and the other received water ad libitum. A stereotaxic surgery was realized for administering (7.5 nmol/rat) of 8-OH-DPAT and (2nmol/rats) WAY100135 intra- DRN. The animals received systemic WAY100135 (5 mg / kg, ip). Interestingly, microinjection of 8-OH-DPAT into the DRN raised an additional long-lasting increase of 0.3 M NaCl intake in sodium-depleted rats despite a high volume ingested 30 min after central injection. Conversely, repeated intra-DRN microinjection (7.5 nmol/rat) evoked a significant long-term decrease in 0.3 M NaCl intake in basal conditions and sodium-depleted rats. Administration of WAY100135 did not alter the responses of ingestion of water or 0.3 M NaCl in the group with no access to water. On the other hand, the 5-HT1A antagonist promoted intense and long-term reduction in the natriorexigenic response, in the group that received water ad libitum. Acute administration of 5-HT1A antagonist significantly decreased de 0.3 M NaCl ingestion in modified FUROCAP and modified beta-adrenergic protocols rats . This response possibly demanded an increased 5-HT activity during salt satiety signaling along the consummatory phase. These results show a clear-cut involvement of the DRN 5-HT1A somatodendritic autoreceptors in sodium satiety signaling under basal conditions and during the consummatory phase of salt intake in sodium-depleted rats.