Behavior Genetics

, Volume 25, Issue 6, pp 569-579

First online:

Influence of dystrophin-gene mutation onmdx mouse behavior. I. Retention deficits at long delays in spontaneous alternation and bar-pressing tasks

  • Cyrille VaillendAffiliated withLaboratoire de Psychophysiologie, ULP, URA CNRS 1295
  • , Alvaro RendonAffiliated withLaboratoire Laveran, Clinique Ophtalmologique, CJF INSERM 92-02
  • , René MisslinAffiliated withLaboratoire de Psychophysiologie, ULP, URA CNRS 1295
  • , Arielle UngererAffiliated withLaboratoire de Psychophysiologie, ULP, URA CNRS 1295

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X-linked Duchenne muscular dystrophy (DMD) is frequently associated with a nonprogressive, cognitive defect attributed to the absence of dystrophin in the brain of DMD patients. The mutantmdx mouse, lacking in 427-kDa dystrophin in both muscle and brain tissues, is considered to be a valuable model of human DMD. In the present study, we comparedmdx and C57BL/10 control mice and showed thatmdx mice had impaired retention in a T-maze, delayed spontaneous alternation task 24 h, but not 6 h, after acquisition.mdx mice were not impaired in acquisition of a bar-pressing task on 4 consecutive days but showed poor retention 22 days after the last training session. Mutants and controls showed similar behavioral responses in free exploration and light/dark choice situations and did not differ in spontaneous locomotor activity or motor coordination. Retention impairments at long delays inmdx mice suggest a role of dystrophin in long-term consolidation processes.

Key Words

Dystrophin gene mutation mdx mouse operant learning delayed spontaneous alternation novelty reaction anxiety motor activity