Influence of dystrophin-gene mutation on mdx mouse behavior. I. Retention deficits at long delays in spontaneous alternation and bar-pressing tasks.
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 mutant mdx 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 compared mdx and C57BL/10 control mice and showed that mdx 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 in mdx mice suggest a role of dystrophin in long-term consolidation processes.
Laboratoire de Psychophysiologie, ULP, URA CNRS 1295, Strasbourg, France.
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Vaillend
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Rendon
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Misslin
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Ungerer
D000818:Animals; D001143:Arousal / Q000235:genetics; D016189:Dystrophin / Q000235:genetics*; D005106:Exploratory Behavior; D008297:Male; D018782:Maze Learning; D011939:Mental Recall; D051379:Mice; D008810:Mice, Inbred C57BL; D018101:Mice, Inbred mdx; D009043:Motor Activity / Q000235:genetics; D009048:Motor Skills; D009137:Muscular Dystrophy, Animal / Q000235:genetics*; D011930:Reaction Time / Q000235:genetics*; D012153:Retention, Psychology
D016189:Dystrophin