Excitatory amino acids in epilepsy.

Epilepsy has been described as a neurological disorder with a prevalence rate estimated at approximately 0.5% of population. In recent years there have been significant advances in our understanding of the contribution of excitatory glutamatergic transmission to seizures. Glutamate appeared to participate in the initiation, propagation and maintenance of epileptic activity. In epileptic patients, changes in glutamate concentration and receptor function were found. Intracerebral or systemic administration of glutamate receptor agonists has become a popular way to induce seizures in rodents. Glutamate antagonists were shown to be potent anticonvulsants in varying experimental seizure models determined genetically, induced chemically and electrically, or due to kindling. A potential therapeutic role for drugs affecting glutamatergic mechanisms in epilepsy has not yet been defined but is constantly attracting interest. In this review we summarize data from studies performed in humans and animals and focus on iono- and metabotropic excitatory amino acid receptor-mediated events in seizures and epilepsy.