These mice show a reduction of dendritic spine density, impaired long-term potentiation, and facilitated long-term depression in the hippocampus, in addition to the loss of the astrocyte glutamate transporters GLT-1 (EAAT2) and GLAST (EAAT1), and decreased glutamate uptake, resulting in a higher sensibility to glutamate excitotoxicity, that is one of the possible pathogenic mechanism in ALS (Figure 2) [62]. The gene discussed is SLC1A2; the disease is amyotrophic lateral sclerosis.