SLC1A2 and amyotrophic lateral sclerosis: Subsequent exogenous delivery of miR-124a in vivo through into spinal cord of ALS mice significantly prevented further pathological loss and led to a 30% increase in the expression of the excitatory amino acid transporter 2 (EAAT2, rodent analog GLT1), which is responsible for the uptake of glutamate from the synaptic cleft (Morel et al., 2013).