The influence of calcium channel blockers on the brain free fatty acid level and glutathione peroxidase activity in rats with lithium and pilocarpine‐induced status epilepticus

Abstract

AbstractThe aim of this study was to investigate possible therapeutic approach to neuronal damage caused by status epilepticus. The effects of the L‐type voltage‐sensitive calcium channel blockers (nimodipine, nicardipine) and NMDA blockers (ifenprodil and MK‐801) on the brain free fatty acid (FFA) level and glutathione peroxidase (GPX) activity in rats with lithium and pilocarpine (LiPi) ‐ induced status epilepticus were examined. Vehicle or various doses of calcium channel and NMDA blockers had been injected i.p. 30 min after the pilocarpine application. Tested doses of nicardipine and MK‐801 did not influence the increase in the brain FFA level. Nimodipine and ifenprodil revealed a tendency to reduce FFA level. The inhibition of L‐type voltage‐sensitive Ca2+ channels or NMDA receptor ‐ associated channels was not sufficient for significant attenuation of an increase in the rat brain FFA content and a decrease GPX activity associated with LiPi ‐ induced status epilepticus. Individual compounds have shown to prevent FFA increase, suggesting some alternative or additional mechanism of action. The prevention of FFA accumulation was not followed by the prevention of GPX decrease indicating the activation of non FFA‐related mechanisms of cell damage.