title: Characterization of monoamine oxidase activity during early stages of quail embryogenesis.
abstract: Catecholamines and other biogenic amines may play a role in early embryogenesis in addition to functioning as neurotransmitters after neuronal differentiation. Regulation of amine levels is mediated by several different parameters including activity levels of degradative enzymes. Since monoamine oxidase (EC 1.4.3.4) is the primary degradative enzyme for these biogenic amines, we have begun to characterize MAO activity during quail embryogenesis. Our results demonstrate that MAO activity is present at all stages of development examined (stages 2-22) and that the MAO specific activity levels are highest during the earliest stages (stages 2-6). Two types of MAO activity similar to adult avian and mammalian MAO-A and MAO-B have been demonstrated by differential clorgyline sensitivity of tryptamine deamination. In addition, SDS-PAGE of embryonic quail [(3)H]pargyiine-labeled MAO demonstrates that the quail MAO-A and MAO-B flavin-containing subunits have apparent molecular weights of 63,000 and 62,000 respectively. We have begun to assess the functional significance of embryonic quail MAO activity by daily injection of MAO inhibitors (clorgyline or clorgyline plus deprenyl) into fertilized eggs. Clorgyline injection selectively and completely inhibited MAO-A activity, while injection of clorgyline and deprenyl inhibited both MAO-A and MAO-B activities when embryos were assayed after either 2 or 7 days of embryonic development. This paradigm will allow a detailed examination of the effects of MAO inhibition on the developing embryo.
authors.affiliation: Department of Human Genetics, Yale University School of Medicine, 333 Cedar Street, New Haven, U.S.A.
authors.forename: J E
authors.initials: JE
authors.lastname: Pintar
authors.affiliation: Department of Anatomy, University of Connecticut Health Center, Farmington, CT 06032, U.S.A.
authors.forename: G D
authors.initials: GD
authors.lastname: Maxwell
authors.affiliation: Department of Human Genetics, Yale University School of Medicine, 333 Cedar Street, New Haven, U.S.A.
authors.forename: X O
authors.initials: XO
authors.lastname: Breakefield