Central regulation of soidum consumption: oxytocinergic and serotoninergic role

GODINO, A., DE LUCA, ANTUNES-RODRIGUES, J. AND L. VIVAS.

Ribeirao Preto, Brasil

Simposio; International Symposium of Neuroendocrinologia. Neuroendocrine control of body fluid homeostasis: Past,present and Future.; 2006

Central regulation of sodium consumption: oxytocinergic and serotoninergic role.Andrea Godino, Laurival A. De Luca, Jr., José Antunes-Rodrigues and Laura Vivas. Instituto de Investigación Médica M. y M. Ferreyra, Córdoba, Argentina. Our previous studies suggest the participation of serotonergic and oxytocinergic neural circuit in the regulation of sodium appetite consummatory phase. Both groups, the serotonergic dorsal raphé nucleus (DRN) cells and oxytocinergic supraoptic and paraventricular nuclei cells, were activated after induced sodium ingestion as shown by increased number of double immunolabeled cells for Fos (marker of neural activity) and serotonin or oxytocin, respectively. Nevertheless, after sodium depletion only the activity of serotonergic DRN cells changes and it was significantly lower compared with control animals, (in normal sodium balance), or depleted animals in the process of restoring sodium balance, by consuming NaCl. Our results are consistent with the idea that there is a tonic inhibition of sodium appetite by serotonergic cells of the raphé nucleus.  Such an inhibitory influence would probably be reduced in the state of sodium deficiency and increased when the animals ingest NaCl and restore body sodium balance. This system is therefore likely to prevent excess NaCl consumption and its activity may be seen as a “satiety marker”. The oxytocinergic system on the other hand, have been involved  in the processing of hyperosmotic signals in different animal models and in our study only induced sodium consumption was associated with enhanced expression of c-fos. This talk will discuss some recent experimental evidence focus on discriminate whether the activation of the serotonergic and oxytocinergic neurons, previously described in our studies, it might be considered a consequence of sodium satiation processes or may be the result of either orosensory stimulation produced by 2% NaCl, or the postingestive consequences such as, stimulation of gastric, hepatoportal sodium sensors.