In mouse models of HD, expression of mutant Huntingtin (mHTT) in astrocytes leads to decrease in the expression of the glutamate transporter [5], and the failure to buffer extracellular potassium and glutamate leads to neuronal hyper-excitability and a HD-like phenotype, which is reversed by restoration of astrocytic membrane conductance [53]. Here, HTT is linked to Huntington disease.