Neuronal frontal cortex and hippocampus glutamate uptake in prehepatic portal hypertensive rats.

MG CHELUJA, AM FERNÁNDEZ, D ROSELLO, MJ SCOLARI, JC PERAZZO , A LEMBERG , GB ACOSTA

Mar del Plata, 9-11 de Noviembre

Congreso; XXXVII Reunión Científica Anual de la Asociación Argentina de Farmacología Experimental (SAFE).; 2005

SAFE

Portal hypertension constitutes a major complication of human and animal cirrhosis that frequently leads to central nervous system (CNS) dysfunction. This pathology creates difficulties to splanchnic circulation across liver parenquimal vasculature, to reach cava vein. A second important syndrome in this pathology is hepatic encephalopathy (sub clinical or ouvert). Here, we  examined the influence on prehepatic portal (PH) rats on synaptic activity of glutamate (Glu) transporters in neuronal frontal cortex (CF) and hippocampus (Hic). PH was produced by performing a calibrated stenosis of portal vein as described by Lores-Arnais (2005). The animals were sacrified by decapitation 14 days after portal vein stenosis. Synaptosomes from CF and Hic were freshly prepared for determination of the  time  course for Glu uptake in Krebs Ringer buffer at 30ºC for different periods up to 30 min. It was documented a statistical significance decrease more Hic than CF in PH rats against sham. We conclude that the HP hipertensive rats  decrease the uptake of Glu in CF and Hic suggesting that it represent toxic levels of Glu in rat brain.