No significant changes in immunohistochemical expression compared to the control group were observed for the glutamate transporter of neuronal origin (GLAST) and the glutamate transporter of glial origin (GLT1), which does not exclude the involvement, especially with the observed chronic neuronal damage, of the existence of synaptic glutamate deficiencies leading—as in schizophrenia—to psychiatric disorders [31]. This evidence concerns the gene SLC1A2 and psychiatric disorder.