| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 4314229 | Behavioural Brain Research | 2010 | 7 Pages |
Several reports have revealed a high density of 5-HT1A receptors in the lateral septal area (LSA), as well as a subpopulation of oxytocin (OT) receptors. Increasing evidence shows that 5-HT1A and OT neurons inhibit sodium urinary excretion. The aim of this study was to investigate the part played by serotonergic (5-HT1A) and oxytocinergic receptors in the LSA in the sodium intake induced in rats by sodium depletion followed by 24 h 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 μg/0.2 μL) reduced 1.8% NaCl solution intake, but injections (1, 2, and 4 μg/0.2 μL) of 8-OH-DPAT, a 5-HT1A agonist, were more effective than 5-HT in reducing 1.8% NaCl intake. Pretreatment of the LSA with the 5-HT1A 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(CH2)5[Tyr(Me)2Thr4, Orn5, Tyr(NH2)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-HT1A serotonergic receptors in the LSA, including some that interact with the oxytocinergic system, modulate sodium intake induced by sodium loss in rats.
