1. Influence of dystrophin-gene mutation onmdx mouse behavior. I. Retention deficits at long delays in spontaneous alternation and bar-pressing tasks
- Author
-
René Misslin, Arielle Ungerer, Cyrille Vaillend, Alvaro Rendon, Neurobiologie de l'apprentissage, de la mémoire et de la communication (NAMC), Université Paris-Sud - Paris 11 (UP11)-Centre National de la Recherche Scientifique (CNRS), Laboratoire d'Ethologie et de Neurobiologie, URA CNRS 1295, and Université Louis Pasteur - Strasbourg I
- Subjects
Male ,mdx mouse ,[SDV.NEU.NB]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Neurobiology ,Duchenne muscular dystrophy ,MESH: Mental Recall ,medicine.disease_cause ,MESH: Muscular Dystrophy, Animal ,MESH: Synapses ,Dystrophin ,Mice ,0302 clinical medicine ,MESH: Animals ,Genetics (clinical) ,0303 health sciences ,Mutation ,[SDV.NEU.PC]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Psychology and behavior ,biology ,MESH: Mice, Inbred mdx ,Retention, Psychology ,[SDV.NEU.SC]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Cognitive Sciences ,Cognition ,Spontaneous alternation ,musculoskeletal system ,MESH: Motor Activity ,Motor coordination ,Motor Skills ,MESH: Exploratory Behavior ,Arousal ,Psychology ,musculoskeletal diseases ,congenital, hereditary, and neonatal diseases and abnormalities ,MESH: Space Perception ,Motor Activity ,03 medical and health sciences ,MESH: Dystrophin ,MESH: Mice, Inbred C57BL ,Reaction Time ,Genetics ,medicine ,Animals ,Maze Learning ,MESH: Mice ,Ecology, Evolution, Behavior and Systematics ,030304 developmental biology ,MESH: Arousal ,MESH: Maze Learning ,MESH: Retention, Psychology ,Muscular Dystrophy, Animal ,medicine.disease ,Dystrophin gene ,MESH: Male ,MESH: Reaction Time ,Mice, Inbred C57BL ,Mental Recall ,Exploratory Behavior ,Mice, Inbred mdx ,biology.protein ,Neuroscience ,030217 neurology & neurosurgery ,MESH: Motor Skills - Abstract
International audience; 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.
- Published
- 1995
- Full Text
- View/download PDF