摘要
Injuries to spinal motoneurons manifest in a variety of forms,including damage to peripheral axons,neurodegenerative disease,or direct insult centrally.Such injuries produce a variety of negative structural and functional changes in both the directly affected and neighboring motoneurons.Exercise is a relatively simple behavioral intervention that has been demonstrated to protect against,and accelerate recovery from,these negative changes.In this article,we describe how exercise is neuroprotective for motoneurons,accelerating axon regeneration following axotomy and attenuating dendritic atrophy following the death of neighboring motoneurons.In both of these injury models,the positive effects of exercise have been found to be dependent on gonadal hormone action.Here we describe a model in which exercise,hormones,and brain-derived neurotrophic factor might all interact to produce neuroprotective effects on motoneuron structure following neural injury.
Injuries to spinal motoneurons manifest in a variety of forms, including damage to peripheral axons, neurodegenerative disease, or direct insult centrally. Such injuries produce a variety of negative structural and functional changes in both the directly affected and neighboring motoneurons. Exercise is a relatively simple behavioral intervention that has been demonstrated to protect against, and accelerate recovery from, these negative changes. In this article, we describe how exercise is neuroprotective for motoneurons, accelerating axon regeneration following axotomy and attenuating dendritic atrophy following the death of neighboring motoneurons. In both of these injury models, the positive effects of exercise have been found to be dependent on gonadal hormone action. Here we describe a model in which exercise, hormones, and brain-derived neurotrophic factor might all interact to produce neuroprotective effects on motoneuron structure following neural injury.
基金
supported by NIH-NINDS NS047264 to DRS
