Alterations of serotonin neurotransmission and inhibition of mouse killing behavior: II. Effects of selective and reversible monoamine oxidase inhibitors of type A

Three groups of rats were tested for mouse killing behavior after IP injection of selective and reversible type A Monoamine Oxidase inhibitors. The rats were either spontaneous killers, or non-killers which acquired killing behavior following para-chlorophenylalanine treatment or electrolytical destruction of dorsal and median raphe nuclei. Moclobemide (para-chloro-N-(2-morpholinoethyl)-benzamide), cimoxatone (3-(4-(3-cyanophenyl-methoxy)phenyl)-5-(methoxy-methyl)-2-oxazo lid inone, MD 780515), toloxatone (5-(hydroxymethyl)-3-(3-methylphenyl)-2-oxazolidinone) and amiflamine ((+)-4-dimethylamino-2, alpha-dimethylphenethyl amine, FLA 336 (+)) were used as selective and reversible Monoamine Oxidase inhibitors of type A. Cimoxatone, toloxatone and amiflamine inhibited mouse killing behavior of spontaneous killer rats without apparent sedation, whereas moclobemide was not efficient at doses which did not decrease locomotor activity. A similar inhibition of mouse killing behavior was obtained in spontaneous and serotonin depleted killer rats. The results are discussed in relation to the behavioral expression of serotoninergic supersensitivity in the three groups of killer rats described earlier using serotonin agonist and uptake inhibitors.