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

Autor: René Misslin, Arielle Ungerer, Cyrille Vaillend, Alvaro Rendon
Přispěvatelé: 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, Université Louis Pasteur - Strasbourg I
Rok vydání: 1995
Předmět:
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
Zdroj: Behavior Genetics
Behavior Genetics, Springer Verlag, 1995, 25 (6), pp.569-579. ⟨10.1007/bf02327580⟩
ISSN: 1573-3297
0001-8244
DOI: 10.1007/bf02327580
Popis: 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.
Databáze: OpenAIRE