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Vitamin A depletion alters sensitivity of motor behavior to MK-801 in C57BL/6J mice

BACKGROUND: Vitamin A and its derivatives (retinoids) are crucial for the development, maintenance and morphogenesis of the central nervous system (CNS). Although motor impairment has been reported in postnatal vitamin A depletion rodents, the effect of vitamin A depletion on homeostasis maintaining...

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Detalles Bibliográficos
Autores principales: Zhang, Ming, Ji, Baohu, Zou, Hong, Shi, Junwei, Zhang, Zhao, Li, Xingwang, Zhu, Hui, Feng, Guoyin, Jin, Meilei, Yu, Lei, He, Lin, Wan, Chunling
Formato: Texto
Lenguaje:English
Publicado: BioMed Central 2010
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2832782/
https://www.ncbi.nlm.nih.gov/pubmed/20180994
http://dx.doi.org/10.1186/1744-9081-6-7
Descripción
Sumario:BACKGROUND: Vitamin A and its derivatives (retinoids) are crucial for the development, maintenance and morphogenesis of the central nervous system (CNS). Although motor impairment has been reported in postnatal vitamin A depletion rodents, the effect of vitamin A depletion on homeostasis maintaining capability in response to external interference is not clear. METHODS: In the current study, we measured the effect of vitamin A depletion on motor ability and pain sensitivity under two different conditions: 1. prior to any injection and 2. after the injection of an N-methyl-D-aspartate (NMDA) receptor antagonist (MK-801). RESULTS: Vitamin A depletion mice showed decreased body weight, enhanced locomotor activity, increased rearing and less tail flick latency. Vitamin A depletion also induced hypersensitivity of stereotypy, ataxia, rearing, and tail flick latency to MK-801, but hyposensitivity of locomotion to MK-801. CONCLUSIONS: These findings suggest that vitamin A depletion affect broad basal behavior and disrupt homeostasis maintaining capability in response to glutamate perturbation. We provide a useful animal model for assessing the role of vitamin A depletion in regulating animal behavior, and for detecting how neurotransmitter pathways might be involved in vitamin A depletion related behavioral abnormalities.