作者: Yves Sagot , Thierry Rossé , Richard Vejsada , Daniel Perrelet , Ann C. Kato
DOI: 10.1523/JNEUROSCI.18-03-01132.1998
关键词:
摘要: It has been shown that abnormalities in axonal transport occur several mouse models with motoneuron degeneration and also the human disease amyotrophic lateral sclerosis. In this report, we have examined potential of neurotrophic factors to act on properties a mutant, progressive motor neuronopathy (pmn). This mutant characterized as “dying-back” motoneuronopathy, loss cell bodies fibers. Retrograde spinal cord motoneurons was determined using fluorescent tracers either injected into gastrocnemius muscle or applied directly onto cut sciatic nerve. Because rate retrograde labeling significantly reduced pmn, compensate for impairment. Ciliary factor (CNTF), brain-derived (BDNF), neurotrophin-3 (NT-3) but not glial-derived (GDNF) nerve growth (NGF) were capable improving labeling. The differential effects these agree previous studies showing molecules promote survival do necessarily deficiency. impairment appears an early event pathology, our results may important clinical implications treatment diseases.