For instance, a switch to CP-AMPAR (lacking GluA2 or containing unedited GluA2) increases neuronal excitability in the hypothalamus of hypertensive rats [67], in the hippocampus of mice with seizures [68], in spinal dorsal horn neurons of rats with inflammatory pain [69,70], and also in differentiated human MNs in amyotrophic lateral sclerosis model [71]. The gene discussed is CP; the disease is amyotrophic lateral sclerosis.