Influence of dystrophin-gene mutation onmdx mouse behavior. I. Retention deficits at long delays in spontaneous alternation and bar-pressing tasks
- Cite this article as:
- Vaillend, C., Rendon, A., Misslin, R. et al. Behav Genet (1995) 25: 569. doi:10.1007/BF02327580
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.