SEARCH

SEARCH BY CITATION

Abstract

The catabolic pathways for dopamine degradation in the goldfish brain and pituitary were investigated. The major dopamine catabolite formed in vivo after L-dihydroxyphenylalanine or dopamine injection was dihydroxyphenylacetic acid. Homovanillic acid and 3-methoxytyramine are also formed but to a much lesser extent. In vitro studies also indicate that the major dopamine catabolite produced by pituitary tissue is dihydroxyphenylacetic acid. Pargyline at a dose which, in mammals, inhibits both monoamine oxidase A and B, and clorgyline at a dose which inhibits monoamine oxidase A, elevates dopamine concentrations in goldfish pituitary. Deprenyl at a dose which inhibits mammalian monoamine oxidase B or dinitrocatechol (OR-468) which inhibits catechol-O-methyltransferase had no effects on pituitary dopamine concentrations in goldfish. Basal serum gonadotropin concentrations are reduced by injection of monoamine oxidase inhibitors but not by injection of the catechol-O-methyltransferase inhibitor. The neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), which appears to require monoamine oxidase for its activity, selectively depletes noradrenaline and dopamine in the goldfish brain and pituitary. Intraperitoneal injection of large amounts of the catecholestrogens 2-hydroxyestradiol or 4-hydroxyestradiol (1 μg/g each hour for 5 hours) has no effect on brain or pituitary dopamine concentrations or serum gonadotropin levels. Catecholestrogens are normally not detectable in goldfish brain and pituitary; however, following intraperitoneal injection substantial amounts are measurable in the brain and pituitary. © 1992 Wiley-Liss, Inc.