Studies on opioid peptides as endogenous anticonvulsants.

In both normal and hypophysectomized rats, electroconvulsive shock (ECS) produced a significant postictal rise in seizure threshold (S.T.) to flurothyl, a volatile convulsant. This ECS-induced increase in S.T. was markedly attenuated by naloxone (10 mg/kg s.c.), which itself did not alter basal S.T. A dose of bicuculline (0.1 mg/kg i.p.) which was slightly proconvulsant in the flurothyl test did not significantly alter the postictal rise in S.T. produced by ECS. With hypophysectomized rats, there was a 24% increase in basal S.T. to flurothyl challenge. Hypophysectomy had no influence on the postictal rise in S.T. produced by ECS, nor on the attenuation that occurs with naloxone. We propose that the postictal rise in S.T. reflects a change occurring centrally which prevents a static convulsive state, possibly through brain opioid peptides acting as endogenous anticonvulsants.