The expression of ARNm and the transporter protein for EAAT-1 and EAAT-2 decrease in acute hyperammonemia (Knecht et al., 1997; Chan and Butterworth, 1999; Felipo and Butterworth, 2002), while extracellular glutamate and glycine concentration increase, generating a neurotoxic environment (Michalak et al., 1998). This evidence concerns the gene SLC1A2 and Hyperammonemia.