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Neuroreport. 2008 May 7;19(7):739-43. doi: 10.1097/WNR.0b013e3282fd6e88.

Novel monoamine oxidase A knock out mice with human-like spontaneous mutation.

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  • 1Department of Pharmacology and Pharmaceutical Sciences, Keck School of Medicine, University of Southern California, Los Angeles, California 90033, USA.

Abstract

A novel line of mutant mice [monoamine oxidase A knockout (MAOA KO)] harboring a spontaneous point nonsense mutation in exon 8 of the MAO A gene was serendipitously identified in a 129/SvEvTac colony. This mutation is analogous to the cause of a rare human disorder, Brunner syndrome, characterized by complete MAO A deficiency and impulsive aggressiveness. Concurrent with previous studies of MAO A KO mice generated by insertional mutagenesis ('Tg8'), MAOA(A863T) KO lack MAO A enzyme activity and display enhanced aggression toward intruder mice. MAOA(A863T) KO, however, exhibited lower locomotor activity in a novel, inescapable open field and similar immobility during tail suspension compared with wild type, observations which differ from reports of Tg8. These findings consolidate evidence linking MAO A to aggression and highlight subtle yet distinctive phenotypical characteristics.

PMID:
18418249
[PubMed - indexed for MEDLINE]
PMCID:
PMC3435113
Free PMC Article

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