Welcome to the new version of CaltechAUTHORS. Login is currently restricted to library staff. If you notice any issues, please email coda@library.caltech.edu
Published March 1987 | public
Journal Article

Differences in Monoamine Oxidase Activity between Cultured Noradrenergic and Cholinergic Sympathetic Neurons

Abstract

Two types of monoamine oxidase activity (MAO-A and MAO-B) help regulate the levels of biogenic amines such as catecholamines and serotonin. Although MAO-A has greater activity toward most catecholamines than MAO-B, no direct experiments have determined the types and levels of MAO activity that are normally expressed in noradrenergic neurons. Noradrenergic neurons from neonatal rat superior cervical ganglia were isolated and cultured under conditions that permit either continued expression of the noradrenergic phenotype or promote a transition to a predominately cholinergic phenotype. After 14–21 days in vitro, neurons from both types of cultures were assayed for the type and amount of monoamine oxidase activity using tryptamine, a common substrate for both MAO-A and MAO-B. Neurons cultured under noradrenergic conditions expressed sevenfold greater MAO activity than neurons cultured under cholinergic conditions. Essentially all MAO activity in the noradrenergic cultures was inhibited by preincubation with 10^(−8–)10^(−9) M clorgyline, which indicated that this activity was primarily MAO-A. Cultures grown under cholinergic conditions exhibited 6- to 10-fold lower MAO-A activity and an 8- to 10-fold lower level of catecholamine synthesis from labeled precursors compared to neurons grown under noradrenergic conditions. These results directly demonstrate that high MAO-A activity is expressed in noradrenergic neurons in vitro. The corresponding decreases in both MAO-A specific activity and catecholamine synthesis as neurons become cholinergic in vitro suggest that the expression of the noradrenergic phenotype involves the coordinate regulation of degradative as well as synthetic enzymes involved in catecholamine metabolism.

Additional Information

© 1987 Academic Press, Inc. Received August 12, 1986; accepted in revised form October 28, 1986. The authors are pleased to acknowledge the assistance of Dr. K. J. Sweadner, Dr. E. J. Wolinsky, and Carmela Castiglione. This work was supported by NIH Grants HD-18592 (J.P.) and NS12105 (X.O.B.), and a grant from NINCDS to P.H.P. J.P. is the recipient of an Irma T. Hirsch Career Scientist Award; P.H.P. and X.O.B. are recipients of McKnight Foundation Neuroscience Development Awards; and P.H.P. was a Rita Allen Foundation Scholar.

Additional details

Created:
August 19, 2023
Modified:
October 18, 2023