THE PRECISE MECHANISM BY WHICH TIAGABINE EXERTS ITS ANTISEIZURE EFFECT IS UNKNOWN, ALTHOUGH IT IS BELIEVED TO BE RELATED TO ITS ABILITY TO ENHANCE THE ACTIVITY OF GAMMA AMINOBUTYRIC ACID (GABA), THE MAJOR INHIBITORY NEUROTRANSMITTER IN THE CENTRAL NERVOUS SYSTEM. THESE EXPERIMENTS HAVE SHOWN THAT TIAGABINE BINDS TO RECOGNITION SITES ASSOCIATED WITH THE GABA UPTAKE CARRIER. IT IS THOUGHT THAT, BY THIS ACTION, TIAGABINE BLOCKS GABA UPTAKE INTO PRESYNAPTIC NEURONS, PERMITTING MORE GABA TO BE AVAILABLE FOR RECEPTOR BINDING ON THE SURFACES OF POST-SYNAPTIC CELLS. TIAGABINE HAS BEEN SHOWN TO PROLONG GABA-MEDIATED INHIBITORY POST-SYNAPTIC POTENTIALS.