Biochemical, behavioral, physiologic, and neurodevelopmental changes in mice deficient in monoamine oxidase A or B.
The availability of mutant mice that lack either MAO A or MAO B has created unique profiles in the central and peripheral availability of serotonin, norepinephrine, dopamine, and phenylethylamine. This paper summarizes some of the current known phenotypic findings in MAO A knock-out mice and contrast these with those of MAO B knock-out mice. Differences are discussed in relation to the biochemical, behavioral, and physiologic changes investigated to date, as well as the role played by redundancy mechanisms, adaptational responses, and alterations in neurodevelopment.
Holschneider
D P
DP
Department of Psychiatry and the Behavioral Sciences, USC School of Medicine, Los Angeles, CA 90089, USA.
Chen
K
K
Seif
I
I
Shih
J C
JC
D000818:Animals; D001522:Behavior, Animal / Q000502:physiology*; D015306:Biogenic Monoamines / Q000378:metabolism*; D002490:Central Nervous System / Q000002:abnormalities* / Q000254:growth & development / Q000378:metabolism*; D006801:Humans; D008818:Mice, Neurologic Mutants; D008995:Monoamine Oxidase / Q000172:deficiency* / Q000235:genetics; D009474:Neurons / Q000378:metabolism* / Q000473:pathology; D010641:Phenotype
D015306:Biogenic Monoamines; D008995:Monoamine Oxidase