Anti-Nogo-A antibody treatment does not prevent cell body shrinkage in the motor cortex in adult monkeys subjected to unilateral cervical cord lesion.
Anti-Nogo-A antibody treatment does not prevent cell body shrinkage in the motor cortex in adult monkeys subjected to unilateral cervical cord lesion.
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抗Nogo-A抗体治疗不会阻止受单侧颈脊病变的成年猴子运动皮层的细胞体收缩。
DOI：
10.1186/1471-2202-9-5
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发表时间：
2008-01-14
期刊：
影响因子：
2.4
通讯作者：
Rouiller, Eric M.
中科院分区：
文献类型：
--
作者：
Beaud, Marie-Laure;Schmidlin, Eric;Wannier, Thierry;Freund, Patrick;Bloch, Jocelyne;Mir, Anis;Schwab, Martin E.;Rouiller, Eric M.
在C7/C8交界处的单侧颈髓损伤阻断成年猴的背外侧索后，使用特定的单抗中和Nogo-A促进了损伤侧和尾侧的皮质脊髓(CS)轴突的萌发，同时促进了功能恢复。在受损但未经抗Nogo-A抗体治疗的猴子中，对侧初级运动皮质(M1)中的CS神经元存活到轴突切断，但它们的胞体缩小。由于抗Nogo-A治疗诱导CS轴突再生和/或萌发，它可能会改善对神经营养因子的获取。因此，问题是，抗NOGO-A治疗是否能阻止在对侧M1观察到的胞体收缩？使用标记SMI-32，对M1的V层锥体神经元(包括CS细胞)进行了定量和定性的解剖学评估，并在三组动物中进行了比较：完整的猴子(n=5)；受到颈髓损伤并接受对照抗体治疗的猴子(n=4)；患有颈髓病变并接受抗Nogo-A抗体治疗的猴子(n=5)。损伤对侧的Smi-32阳性神经元通常比患侧大脑半球的Smi-32阳性神经元染色更浅，这表明它们表达的神经丝较少。然而，在所有三组猴子中，Smi-32阳性神经元在两个半球的数量大致相当，证实了大多数被切断轴突的CS神经元存活的观点。但两组损毁猴的对侧大脑半球CS胞体面积均有缩小。在用抗Nogo-A抗体处理的猴子中，发现细胞表面收缩的程度与用对照抗体处理的猴子相同。抗Nogo-A抗体处理不能防止轴突细胞胞体收缩，说明抗Nogo-A抗体处理主要在远端水平影响轴突切断的CS神经元，尤其是在颈髓的轴突侧化，而在其胞体水平上影响很少或根本不影响。
After unilateral cervical cord lesion at the C7/C8 border interrupting the dorsolateral funiculus in adult monkeys, neutralization of Nogo-A using a specific monoclonal antibody promoted sprouting of corticospinal (CS) axons rostral and caudal to the lesion and, in parallel, improved functional recovery. In monkeys lesioned but not treated with the anti-Nogo-A antibody, the CS neurons in the contralesional primary motor cortex (M1) survived to the axotomy, but their soma shrank. Because the anti-Nogo-A treatment induces regeneration and/or sprouting of CS axons, it may improve access to neurotrophic factors. The question therefore arises as to whether anti-Nogo-A treatment prevents the soma shrinkage observed in the contralesional M1? Using the marker SMI-32, a quantitative and qualitative anatomical assessment of the pyramidal neurons in the layer V (thus including the CS cells) in M1 was performed and compared across three groups of animals: intact monkeys (n = 5); monkeys subjected to the cervical cord lesion and treated with a control antibody (n = 4); monkeys with the cervical lesion and treated with anti-Nogo-A antibody (n = 5). SMI-32 positive neurons on the side contralateral to the lesion were generally less well stained than those on the ipsilesional hemisphere, suggesting that they expressed less neurofilaments. Nevertheless, in all three groups of monkeys, the amount of SMI-32 positive neurons in both hemispheres was generally comparable, confirming the notion that most axotomized CS neurons survived. However, shrinkage of CS cell body area was observed in the contralesional hemisphere in the two groups of lesioned monkeys. The cell surface shrinkage was found to be of the same magnitude in the monkeys treated with the anti-Nogo-A antibody as in the control antibody treated monkeys. The anti-Nogo-A antibody treatment did not preserve the axotomized CS cells from soma shrinkage, indicating that the anti-Nogo-A antibody treatment affects morphologically the axotomized CS neurons mainly at distal levels, especially the axon collateralization in the cervical cord, and little or not at all at the level of their soma.
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