Affiliations: Department of Pharmacology and Toxicology, University
Medical School, Jaczewskiego 8, PL-20-090, Lublin, Poland | Department of Clinical Toxicology, Institute of
Agricultural Medicine, Jaczewskiego 2, PL-20-950, Lublin, Poland
Note: [] Corresponding author: E.M. Urbanska, Department of
Pharmacology and Toxicology, University Medical School, Jaczewskiego 8,
PI-20-090 Lublin, Poland. Tel.: +48 81 747 8373; Fax: +48 81 747 8924; E-mail:
ewau@galen.imw.lublin.pl
Abstract: 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.
