Dysregulation of GATs in the basal ganglia, including on astrocytes, has now been implicated in several models of neurological disease: in 6-OHDA toxin-based rat and mouse models of dopamine depletion in Parkinson’s, astrocytes in the external globus pallidus have downregulated GAT-344; and in R6/2 and FVB/N transgenic mouse models of Huntington’s disease, striatal GAT expression is increased and tonic inhibition by ambient GABA decreased15,27, with one recent study directly implicating GATs on astrocytes in this mechanism23. This evidence concerns the gene GLYAT and juvenile Huntington disease.