Dopamine catabolism in goldfish (Carassius auratus) brain and pituitary: Lack of influence of catecholestrogens on dopamine catabolism and gonadotropin secretion

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.