SLC1A3 and Hyperammonemia: These results are in sharp contrast to the reported GLAST/EAAT1 reduction in brain tissue in hyperammonemia and HE without liver disease, where a transitory down-regulation of GLAST, and increase of extracellular Glu is followed by an upregulation mechanism to counteract the excitotoxicity of Glu levels (Norenberg et al., 1997; Butterworth, 2002; Ochoa-Sanchez and Rose, 2018).