SLC6A1 and juvenile absence epilepsy: Notably, in some mouse and rat genetic models of absence seizure, including the GAERS rats and the stargazer mice, the combined NRT- and SNr-derived ictal increase in GABAergic inhibition of thalamocortical neurons may be enhanced by the loss-of-function of the astrocytic GABA transporter GAT-1 (but not GAT-3) (Cope et al., 2009; Pirttimaki et al., 2013), providing additional restraints to the thalamocortical neuron firing.