Jablonka Sibylle, Karle Kathrin, Sandner Beatrice, Andreassi Catia, von Au Katja, Sendtner Michael
Institute for Clinical Neurobiology, Josef-Schneider-Str. 11, D-97080 Wuerzburg, Germany.
Hum Mol Genet. 2006 Feb 1;15(3):511-8. doi: 10.1093/hmg/ddi467. Epub 2006 Jan 5.
Motor neuron degeneration is the predominant pathological feature of spinal muscular atrophy (SMA). In patients with severe forms of the disease, additional sensory abnormalities have been reported. However, it is not clear whether the loss of sensory neurons is a common feature in severe forms of the disease, how many neurons are lost and how loss of sensory neurons compares with motor neuron degeneration. We have analysed dorsal root ganglionic sensory neurons in Smn-/-;SMN2 mice, a model of type I SMA. In contrast to lumbar motor neurons, no loss of sensory neurons in the L5 dorsal root ganglia is found at post-natal days 3-5 when these mice are severely paralyzed and die from motor defects. Survival of cultured sensory neurons in the presence of NGF and other neurotrophic factors is not reduced in comparison to wild-type controls. However, isolated sensory neurons have shorter neurites and smaller growth cones, and beta-actin protein and beta-actin mRNA are reduced in sensory neurite terminals. In footpads of Smn-deficient mouse embryos, sensory nerve terminals are smaller, suggesting that Smn deficiency reduces neurite outgrowth during embryogenesis. These data indicate that pathological alterations in severe forms of SMA are not restricted to motor neurons, but the defects in the sensory neurons are milder than those in the motor neurons.
运动神经元变性是脊髓性肌萎缩症(SMA)的主要病理特征。在患有严重形式该疾病的患者中,已有额外感觉异常的报道。然而,尚不清楚感觉神经元的丧失是否是严重形式疾病的常见特征、有多少神经元丧失以及感觉神经元的丧失与运动神经元变性相比情况如何。我们分析了I型SMA模型Smn-/-;SMN2小鼠的背根神经节感觉神经元。与腰段运动神经元不同,在出生后3 - 5天,当这些小鼠严重瘫痪并死于运动缺陷时,未发现L5背根神经节中的感觉神经元有丧失。与野生型对照相比,在存在神经生长因子(NGF)和其他神经营养因子的情况下,培养的感觉神经元的存活率并未降低。然而,分离出的感觉神经元的神经突较短且生长锥较小,并且感觉神经突末端的β-肌动蛋白蛋白和β-肌动蛋白mRNA减少。在Smn缺陷型小鼠胚胎的足垫中,感觉神经末梢较小,这表明Smn缺陷会减少胚胎发育过程中的神经突生长。这些数据表明,严重形式SMA的病理改变并不局限于运动神经元,而是感觉神经元中的缺陷比运动神经元中的缺陷更轻微。