Role of serotonergic 5-HT1A and oxytocinergic receptors of the lateral septal area in sodium intake regulation.

Several reports have revealed a high density of 5-HT(1A) receptors in the lateral septal area (LSA), as well as a subpopulation of oxytocin (OT) receptors. Increasing evidence shows that 5-HT(1A) and OT neurons inhibit sodium urinary excretion. The aim of this study was to investigate the part played by serotonergic (5-HT(1A)) and oxytocinergic receptors in the LSA in the sodium intake induced in rats by sodium depletion followed by 24h deprivation. Cannulae were implanted bilaterally into the LSA of rats to enable the introduction of receptor ligands into that brain area. Serotonergic injections of 5-HT (10, 20, and 40 microg/0.2 microL) reduced 1.8% NaCl solution intake, but injections (1, 2, and 4 microg/0.2 microL) of 8-OH-DPAT, a 5-HT(1A) agonist, were more effective than 5-HT in reducing 1.8% NaCl intake. Pretreatment of the LSA with the 5-HT(1A) antagonist pMPPF partially reduced the inhibitory effect of 5-HT and totally reversed the effects of 8-OH-DPAT on 1.8% NaCl intake induced by sodium depletion. Previous treatment with the potent oxytocin receptor antagonist d(CH(2))(5)[Tyr(Me)(2)Thr(4), Orn(5), Tyr(NH(2))(9)]-vasotocin also totally blocked the inhibitory effects of 5-HT or 8-OH-DPAT on 1.8% NaCl intake. These results show that 5-HT(1A) serotonergic receptors in the LSA, including some that interact with the oxytocinergic system, modulate sodium intake induced by sodium loss in rats.