INIMEC - CONICET   05467
INSTITUTO DE INVESTIGACION MEDICA MERCEDES Y MARTIN FERREYRA
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
- Sodium appetite: Why does it not develop immediately after sodium depletion?
Autor/es:
GODINO, ANDREA; CAEIRO XIMENA; VIVAS LAURA
Lugar:
San Diego, USA
Reunión:
Congreso; 40th annual meeting Neuroscience 2010 (SfN); 2010
Resumen:
Sodium appetite: why does it not develop immediately after sodium depletion? Godino A, Caeiro X, Vivas L. Instituto de Investigación Médica Mercedes y Martín Ferreyra INIMEC-CONICET. Córdoba, Argentine.   Sodium appetite (SA), in contrast to thirst, does not develop immediately after hypovolemia or sodium depletion (SD) and even it appears just when the volemia and natremia is reestablished maybe by body sodium reservoirs. Previous studies from this laboratory have shown that acute Na depletion by peritoneal dialysis (PD) produces a rapid and significant drop in Na concentration of serum and CSF within 1-4 hours after PD; rising gradually until 20 hours later when the animals not only recovery the extracellular Na normal values but also the specific Na appetite became evident. We have also investigated the brain areas and neurochemical systems involved in both the appetitive (24hs after PD) and satiety (after induced sodium intake) phases of SA (Franchini et al, 1999, 2002, Godino et al, 2007). In these studies sodium depletion increased neural activity as shown by Fos immunoreactivity (Fos-ir) in the lamina terminalis (LT) areas and decrease Fos expression in  serotonergic neurons of the dorsal raphe nucleus (DRN) suggesting their participation in the genesis of SA. On the other hand, induced hypertonic Na intake increase the Fos-ir in brainstem areas, oxitocinergic (OT) cells at hypothalamic level and serotonergic (5HT) neurons at DRN, indicating their involvement in the inhibition of SA. However, until now we did not know which areas are involved in this delay or temporary dissociation between SD and SA behavior. Taking into account this evidence our aim was to analyze the Fos-ir brain areas 2 hours after PD in rats. In addition, we combined Fos-ir with the specific antibody for OT and 5HT.  Results: we observed a significant increase in the number of Fos-ir neurons in the circunventricular organs of the LT (subfornical organ p= 0.014 and organum vasculosum lamina terminalis p= 0.003), and in the extended amydala structures such as central amygdala (p=0.0015) and bed nucleus of the stria terminalis lateral (p=0.009). Contrary as we expected, we did not observed any increase in the number of  Fos-OT neurons. However, we found an increased number of Fos-ir neurons in the area postrema (p=0.003) nucleus of the solitary tract (p=0.0003) and lateral parabrachial nucleus (p=0.035) areas previously involved in the inhibition of SA. Regarding the Fos-5HT neurons we did not find any significant changes compared to control suggesting that the tonic inhibition of SA continuous at this time. Summary: Based on our results is possible to postulate that this temporary dissociation between the fall of plasma sodium levels and the expression of sodium appetite might be due to simultaneous activation of areas involved in the genesis and inhibition of sodium appetite. Supported by: CONICET and ANPCyT