Godino A, De Luca LA, Jr, Antunes-Rodrigues J, Vivas L. Oxytocinergic and serotonergic systems involvement in sodium intake regulation: satiety or hypertonicity markers? Am J Physiol Regul Integr Comp Physiol 293: R1027-R1036, 2007. First published June 13, 2007; doi:10.1152/ajpregu.00078.2007.-Previous studies demonstrated the inhibitory participation of serotonergic (5-HT) and oxytocinergic (OT) neurons on sodium appetite induced by peritoneal dialysis (PD) in rats. The activity of 5-HT neurons increases after PD-induced 2% NaCl intake and decreases after sodium depletion; however, the activity of the OT neurons appears only after PDinduced 2% NaCl intake. To discriminate whether the differential activations of the 5-HT and OT neurons in this model are a consequence of the sodium satiation process or are the result of stimulation caused by the entry to the body of a hypertonic sodium solution during sodium access, we analyzed the number of Fos-5-HT-and Fos-OTimmunoreactive neurons in the dorsal raphe nucleus and the paraventricular nucleus of the hypothalamus-supraoptic nucleus, respectively, after isotonic vs. hypertonic NaCl intake induced by PD. We also studied the OT plasma levels after PD-induced isotonic or hypertonic NaCl intake. Sodium intake induced by PD significantly increased the number of Fos-5-HT cells, independently of the concentration of NaCl consumed. In contrast, the number of Fos-OT neurons increased after hypertonic NaCl intake, in both depleted and nondepleted animals. The OT plasma levels significantly increased only in the PD-induced 2% NaCl intake group in relation to others, showing a synergic effect of both factors. In summary, 5-HT neurons were activated after body sodium status was reestablished, suggesting that this system is activated under conditions of satiety. In terms of the OT system, both OT neural activity and OT plasma levels were increased by the entry of hypertonic NaCl solution during sodium consumption, suggesting that this system is involved in the processing of hyperosmotic signals. sodium appetite; dorsal raphe nucleus; paraventricular nucleus; supraoptic nucleus; tonicity signals INHIBITORY MECHANISMS OF SODIUM appetite involve oxytocinergic (OT) and serotonergic (5-HT) neurons: hypertonic NaCl intake by sodium-depleted rats activates both groups of neurons as shown, for example, by Fos expression, and increased sodium appetite results when these neurons, their projections, or receptors are inactivated (13,14,29,30,31). However, the inhibitory function of these two systems is not entirely clear. They might be part of a system that prevents cell dehydration by restraining hypertonic solution intake during the expression of sodium appetite in hypovolemic animals, but it is also possible that their activation itself leads to satiety or the termination of sodium appetite.Moreover, each neuronal group may also have its own role within inhibitory systems. For example, sodium depletion and subsequent hypertonic NaCl intake, respectively, decrease and increase Fos expre...
