Abstracts

Rationale: Postictal depression is absent in immature rats, there is postictal potentiation instead of refractoriness. Cortical epileptic afcterdischarges (CxAD) were used to analyze a role of excitatory amino acid transmission in this phenomenon. Methods: Epidural cortical stimulation and recording electrodes were implanted to 12-day-old rat pups. Four CxADs were always elicited by 8-Hz stimulation series lasting 15 s. Interval between stimulations was 1, 10, and 1 min to induce two pairs of CxADs, drugs were injected immediately after the first testing CxAD. Antagonists of NMDA receptors MK-801 (0.1 and 0.5 mg/kg) and ifenprodil (20 and 40 mg/kg) were used. Duration of afterdischarges was measured off-line and statistically evaluated. Results: Control animals injected with saline demonstrated significant prolongation of testing CxADs. Noncompetitive antagonist of NMDA receptors MK-801 (dizocilpine) was able to suppress the prolongation of the testing CxADs in a dose-dependent manner. The lower dose of ifendprodil does not affect the second pair of CxADs but the 40/mg/kg dose decreased the duration of the second conditioning and even more of the second testing CxAD. First experiments with memantine yielded similar results. Conclusions: NMDA receptors play a (probably principal) role in postictal potentiation after cortical epileptic afterdischarges. Not only nonspecific antagonist dizocilpine but also ifenprodil, a specific antagonist of NMDA receptors containing NR2B subunit, are able to block the potentiation of ths testing CxADs. Funding: Supported by US-Czech grants No.LH-11015 and LH-15032