Gamma-aminobutyric acid (GABA), one of the main inhibitory neurotransmitters in 
the brain, interacts with three types of receptors for GABA--GABA(A), GABA(B) 
and GABA(C). GABA(A) receptors, associated with binding sites for 
benzodiazepines and barbiturates in the form of a receptor complex, control 
opening of the chloride channel. When GABA binds to the receptor complex, the 
channel is opened and chloride anions enter the neuron, which is finally 
hyperpolarized. GABA(B) receptors are metabotropic, linked to a cascade of 
second messengers whilst the physiological meaning of ionotropic GABA(C) 
receptors, mainly located in the retina, is generally unknown. Novel 
antiepileptic drugs acting selectively through the GABA-ergic system are 
tiagabine and vigabatrin. The former inhibits neuronal and glial uptake of GABA 
whilst the latter increases the synaptic concentration of GABA by inhibition of 
GABA-aminotransferase. Gabapentin, designed as a precursor of GABA easily 
entering the brain, was shown to increase brain synaptic GABA. This 
antiepileptic drug also decreases influx of calcium ions into neurons via a 
specific subunit of voltage-dependent calcium channels. Conventional 
antiepileptics generally inhibit sodium currents (carbamazepine, phenobarbital, 
phenytoin, valproate) or enhance GABA-ergic inhibition (benzodiazepines, 
phenobarbital, valproate). Ethosuximide, mainly controlling absences, reduces 
calcium currents via T-type calcium channels. Novel antiepileptic drugs, mainly 
associated with an inhibition of voltage-dependent sodium channels are 
lamotrigine and oxcarbazepine. Since glutamate-mediated excitation is involved 
in the generation of seizure activity, some antiepileptics are targeting 
glutamatergic receptors--for instance, felbamate, phenobarbital, and topiramate. 
Besides, they also inhibit sodium currents. Zonisamide, apparently sharing this 
common mechanism, also reduces the concentration of free radicals. Novel 
antiepileptic drugs are better tolerated by epileptic patients and practically 
are devoid of important pharmacokinetic drug interactions.