Selective inhibition of amine oxidases differently potentiate the hypophagic effect of benzylamine in mice.

In mice deprived of food for 12 h, the i.c.v. or i.p. administration of benzylamine, a substrate common to both monoamine oxidase B and semicarbazide-sensitive benzylamine oxidases, dose-dependently inhibited feeding. This effect was significantly potentiated by selective monoamine oxidase A and B inhibition, suggesting that central monoamines, known to be substrates of these enzymes may be released. The i.p. administration of semicarbazide-sensitive benzylamine oxidase inhibitors, B24 (3,5-ethoxy-4-aminomethylpyridine) and MDL 72274 ((E)-2-phenyl-3-chloroallylamine) strongly potentiated the effect of i.p. but not i.c.v.-administered benzylamine. The hypophagic effect of benzylamine was evaluated following i.c.v. administration, in comparison with the effect of the sympathomimetic compound amphetamine or the K(+) channel blocker tetraethylammonium, as reference compounds. Our results make it possible to define benzylamine as a centrally acting hypophagic compound devoid of amphetamine-like motor stimulatory effects and point to a role of B24 and MDL 72274 as specific peripheral enhancers of the pharmacological effects of benzylamine.