Tsang D, Ho K P, Wen H L
Brain Res. 1986 May;391(2):187-92. doi: 10.1016/0165-3806(86)90282-8.
The development of total monoamine oxidase (MAO) and MAO-A and MAO-B in the forebrain, brainstem, cerebellum and liver of methadone-treated and normal rats were monitored with tryptamine, serotonin and benzylamine, respectively. Daily administration of methadone (10 mg/kg, s.c.) to pregnant and nursing rats substantially retarded the development of total and the A-form of MAO in the brain regions of pups but had no effect on that of MAO-B. The effect of methadone on the development of total MAO and MAO-A in the liver was only transient and less significant. This finding indicates that the perinatal opiate syndrome associated with maternal exposure to methadone is caused by the inhibition in MAO-A development in monoaminergic neurons in the brain.
分别用色胺、5-羟色胺和苄胺监测了美沙酮处理的大鼠和正常大鼠前脑、脑干、小脑及肝脏中总单胺氧化酶（MAO）、MAO-A和MAO-B的发育情况。对怀孕和哺乳期大鼠每日皮下注射美沙酮（10mg/kg），可显著延缓幼崽脑区中总MAO及MAO-A型的发育，但对MAO-B的发育无影响。美沙酮对肝脏中总MAO和MAO-A发育的影响只是暂时的，且不太显著。这一发现表明，与母体接触美沙酮相关的围产期阿片综合征是由脑中单胺能神经元MAO-A发育受到抑制所致。
