GABA Transporter Biology – University of Copenhagen

GABA Transporter Biology

Fig. 1 Schematic representation of a typical GABAergic synapse with cellular localization of GAT1, BGT1, and GAT3

An introduction to our field of research

Epilepsy is one of the most common chronic neurological disorders. It has been suggested that seizure activity is the result of an imbalance between the inhibitory and excitatory neurotransmission – mediated by γ-aminobutyric acid (GABA) and glutamate, respectively – in which the balance is tipped towards the excitatory neurotransmission.

The treatment of epilepsy can be facilitated by: attenuation of excitatory neurotransmission; modulation of voltage-dependent ion-channels; and enhancement of GABAergic neurotransmission. Our research focuses on the latter approach.

It has been proposed that inhibition of GABA transport – particularly the glial GABA transport – can prevent seizures, as has been shown using tiagabine and other novel GABA uptake inhibitors.

GABA transporters

To date, four GABA transporters (GAT) have been cloned and designated GAT1-4, according to the nomenclature used for mouse clones. Our ongoing research is concerned with the pharmacology of these four transporter. The effort to elucidate their interplay in the synapses between neurons and astrocytes is of high priority.