GABAergic gain-of-function in absence seizures

New evidence indicates that increased, rather than decreased, -aminobutyric acid (GABA)ergic inhibition characterizes typical absence seizures. In particular, enhanced tonic GABAA inhibition, resulting from a malfunction of the astrocytic GABA transporter GAT-1, occurs in thalamocortical neurons of all well-established pharmacologic and genetic models. Interestingly, GABAB receptors positively modulate this tonic current. For an expanded treatment of this topic see Jasper’s Basic Mechanisms of the Epilepsies, Fourth Edition (Noebels JL, Avoli M, Rogawski MA, Olsen RW, Delgado-Escueta AV, eds) published by Oxford University Press (available on the National Library of Medicine Bookshelf [NCBI] at http://www.ncbi.nlm.nih.gov/books)