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

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


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.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Aggression / physiology
  • Animals
  • Base Sequence
  • Disease Models, Animal*
  • Genetic Diseases, X-Linked / genetics*
  • Genetic Diseases, X-Linked / physiopathology*
  • Humans
  • Male
  • Mental Disorders / genetics
  • Mice
  • Mice, Knockout
  • Molecular Sequence Data
  • Monoamine Oxidase / genetics*
  • Motor Activity / genetics
  • Point Mutation
  • Polymerase Chain Reaction


  • Monoamine Oxidase