RESUMO
We recently reported that dystrophin-deficient mdx mice exhibited a hypersensitive freezing response to fearful events such as brief restraint. In the present study, we ethologically characterized the restraint-induced freezing response in mdx mice. This response was evident when restrained mdx mice were released into a new cage or their home cage, but it was remarkably reduced in cages in which other individuals (wild-type mice that had never been reared with the tested mice) had been reared (the resident mice were removed prior to testing). Reciprocally, exploratory behaviors of restrained mdx mice were outstandingly enhanced in the cages in which other individuals had been reared, suggesting the possibility that scent deposited by residents induced exploration in mdx mice. These results suggest that restraint-induced freezing response in mdx mice is influenced by the attention state of the mouse.
Assuntos
Comportamento Animal/fisiologia , Distrofina/genética , Camundongos Endogâmicos mdx/psicologia , Estresse Psicológico/genética , Estresse Psicológico/psicologia , Animais , Western Blotting , Química Encefálica/genética , Corticosterona/metabolismo , Comportamento Exploratório/fisiologia , Feminino , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Atividade Motora/fisiologia , Fenótipo , Restrição Física , Caracteres Sexuais , Olfato/genética , Olfato/fisiologiaRESUMO
Duchenne muscular dystrophy (DMD) is secondary to loss-of-function mutations in the dystrophin gene. The causes underlying the progression of DMD, differential muscle involvement, and the discrepancies in phenotypes among species with the same genetic defect are not understood. The mdx mouse, an animal model with dystrophin mutation, has a milder phenotype. This article reviews the available information on expression of signaling-related molecules in DMD and mdx. Extracellular matrix proteoglycans, growth factors, integrins, caveolin-3, and neuronal nitric oxide synthase expression do not show significant differences. Calcineurin is inconsistently activated in mdx, which is associated with lack of cardiomyopathy, compared to the permanent calcineurin activation in mdx/utrophin null mice that have a DMD-like cardiomyopathy. Levels of focal adhesion kinase (FAK) and extracellular regulated kinases (ERKs) differ among mdx and DMD. Further work is needed to identify the point of discrepancy in these signaling molecules' pathways in dystrophynopathies.
