Medvedev A E, Gorkin V Z, Fedotova I B, Semiokhina A F, Glover V, Sandler M
Institute of Biological and Medical Chemistry, Academy of Medical Sciences, Moscow, Russia.
Biochem Pharmacol. 1992 Sep 25;44(6):1209-10. doi: 10.1016/0006-2952(92)90386-w.
Brain tribulin activity in rats with an inherited predisposition to audiogenic epilepsy was studied after seizures of different intensity were induced by an electric bell. Weak seizures (from 0 to 2 arbitrary units) did not produce any changes in endogenous inhibitory activity towards either monoamine oxidase (MAO) A or B. Moderate seizures were characterized by increases in both MAO A and MAO B inhibitory activity (up to 1.9-fold). Complete tonic epileptiform seizures with total areflexia (4 arbitrary units) induced further augmentation (up to 2.5-fold) of MAO A but not of MAO B inhibitory activity. This dissociation between the two inhibitory activities points to the existence of a separate MAO A-inhibiting component of brain tribulin which is different from isatin.