prostaglandin-d2 and Epilepsy--Tonic-Clonic

This study was undertaken to evaluate the role of brain PGD2 activity during PTZ induced seizures in rats. Potentiation of endogenous PGD2 activity caused an anti-convulsant effect. Thus, after PGD2 injection (5 microg/icv) the latency of generalized tonic clonic convulsions was prolonged. ZK 118.182, a stable analogue of PGD2, dose-dependently inhibited the incidence and the intensity of seizures when injected at doses of 1-100 ng/icv. But on the other hand, inhibition of PGD2 activity either by a D-type PG receptor antagonist (AH 6809; 50 ng/icv) or by a PGD synthase inhibitor (sodium selenite; 0.2 microg/icv) produced a proconvulsant effect by increasing the incidence and the intensity of the seizures. These findings indicate that endogenous PGD2 activity in the brain may have a specific inhibitory role for the initiation and propagation of PTZ induced seizures in rats.

Topics: Animals; Anticonvulsants; Cerebral Ventricles; Dinoprost; Epilepsy, Tonic-Clonic; Injections, Intraventricular; Male; Pentylenetetrazole; Prostaglandin Antagonists; Prostaglandin D2; Rats; Rats, Wistar; Seizures; Sodium Selenite; Xanthenes; Xanthones