Desynchronization of electrical activity in rats induced by deprenyl-an inhibitor of monoamine oxidase B- and relationship with selective increase of dopamine and?-phenylethylamine

Abstract

Electrophysiological and biochemical effects of deprenyl andβ-phenylethylamine were studied in rats, d, l-Deprenyl, l-deprenyl (4–16 mg/kg) andβ-phenylethylamine (75 mg/kg) induced a desynchronization of ECoG after i.p. administration of drugs. The effects lasted several hours. The biochemical analysis indicate that d, l-deprenyl (4 mg/kg) nearly doubled the concentration of brain dopamine (DA) while the concentration of noradrenaline was not altered. The maximal increase was reached at 60 min and the enhanced concentration of DA stayed at this level up till 180 min after administration of drug. Treatment of rats withα-methyl-p-tyrosine (200 mg/kg) did not antagonize a deprenyl induced desynchronization of ECoG. However, even low dose of haloperidol (0.1 mg/kg) abolished the arousal effect of d, l-deprenyl andβ-phenylethylamine. It is suggested that desynchronization of EEG induced by deprenyl is more likely due to increased endogenousβ-phenylethylamine than to increased concentration of endogenous DA in the brain.