The catabolism of intracerebroventricularly injected 5-hydroxytryptamine in mouse brain was investigated. Pretreatment of animals with the 5-hydroxytryptamine type 1 receptor antagonist metergoline, the 5-hydroxytryptamine type 2 receptor antagonist ketanserin, the 5-hydroxytryptamine reuptake inhibitor fluoxetine, or the selective 5-hydroxytryptamine neurotoxin 5,7-dihydroxytryptamine failed to alter the rate of catabolism of intracerebroventricularly administered 5-hydroxytryptamine. The monoamine oxidase inhibitor tranylcypromine effectively blocked degradation of injected 5-hydroxytryptamine and accumulation of 5-hydroxyindoleacetic acid. Coinjection of tryptamine with 5-hydroxytryptamine reduced the rate of conversion of 5-hydroxytryptamine to 5-hydroxyindoleacetic acid. These results indicate that intracerebroventricularly administered 5-hydroxytryptamine is removed by a monoamine oxidase dependent system. This catabolism is not affected by inhibition of presynaptic uptake, 5-hydroxytryptamine receptor type 1 or type 2 blockade, or destruction of serotonergic nerve terminals. The coadministration of tryptamine may prolong the residence period of 5-hydroxytryptamine through competition for monoamine oxidase.Key words: 5-hydroxytryptamine, tryptamine, monoamine oxidase, intracerebroventricular injection, catabolism.
Calcineurin-mediated protein dephosphorylation in brain nerve terminals regulates the release of glutamate.
