Epilepsy is characterised by the propensity of the brain to generate spontaneous 
recurrent bursts of excessive neuronal activity, seizures. GABA-mediated 
inhibition is critical for restraining neuronal excitation in the brain, and 
therefore potentiation of GABAergic neurotransmission is commonly used to 
prevent seizures. However, data obtained in animal models of epilepsy and from 
human epileptic tissue suggest that GABA-mediated signalling contributes to 
interictal and ictal activity. Prolonged activation of GABA(A) receptors during 
epileptiform bursts may even initiate a shift in GABAergic neurotransmission 
from inhibitory to excitatory and so have a proconvulsant action. Direct 
targeting of the membrane mechanisms that reduce spiking in glutamatergic 
neurons may better control neuronal excitability in epileptic tissue. 
Manipulation of brain pH may be a promising approach and recent advances in gene 
therapy and optogenetics seem likely to provide further routes to effective 
therapeutic intervention.