GLYAT and Huntington disease: 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.