During early HD stages, several astrocyte dysfunctions have been revealed: (i) reduction of K+ buffering mediated by decrease Kir4.1 channel expression in two mice models (R6/2 and Q175) for HD in striatal astrocytes; and (ii) disrupted intracellular Ca2+ signaling and decreased extracellular uptake of glutamate GLT1-mediated [206,207,208]. Here, SLC1A2 is linked to Huntington disease.