Effect of maternal methadone administration on the development of multiple forms of monoamine oxidase in rat brain and liver.
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.
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D000818:Animals; D001921:Brain / Q000201:enzymology* / Q000254:growth & development; D005260:Female; D007527:Isoenzymes / Q000378:metabolism*; D008099:Liver / Q000201:enzymology*; D008691:Methadone / Q000008:administration & dosage / Q000494:pharmacology*; D008995:Monoamine Oxidase / Q000378:metabolism*; D009293:Opioid-Related Disorders / Q000534:rehabilitation; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D051381:Rats; D011919:Rats, Inbred Strains
D007527:Isoenzymes; D008995:Monoamine Oxidase; D008691:Methadone