Yick L W, Wu W, So K F, Yip H K, Shum D K
Department of Anatomy, Faculty of Medicine, University of Hong Kong, Hong Kong.
Neuroreport. 2000 Apr 7;11(5):1063-7. doi: 10.1097/00001756-200004070-00032.
We examined whether enzymatic digestion of chondroitin sulfate (CS) promoted the axonal regeneration of neurons in Clarke's nucleus (CN) into a peripheral nerve (PN) graft following injury of the spinal cord. After hemisection at T11, a segment of PN graft was implanted at the lesion site. Either vehicle, brain-derived neurotrophic factor (BDNF) or chondroitinase ABC was applied at the implantation site. The postoperative survival period was 4 weeks. Treatment with vehicle or BDNF did not promote the axonal regeneration of CN neurons into the PN graft. Application of 2.5 unit/ml chondroitinase ABC resulted in a significant increase (12.8%) in the number of regenerated CN neurons. Double labeling with Fluoro-Gold and NADPH-diaphorase histochemistry showed that the regenerated CN neurons did not express nitric oxide synthase (NOS). Our results suggest that CS is inhibitory to the regeneration of CN neurons following injury of the spinal cord.
我们研究了脊髓损伤后,硫酸软骨素(CS)的酶解是否能促进克拉克核(CN)神经元轴突再生进入周围神经(PN)移植物。在T11进行半横切后,将一段PN移植物植入损伤部位。在植入部位应用赋形剂、脑源性神经营养因子(BDNF)或软骨素酶ABC。术后存活期为4周。用赋形剂或BDNF治疗并不能促进CN神经元轴突再生进入PN移植物。应用2.5单位/毫升的软骨素酶ABC可使再生的CN神经元数量显著增加(12.8%)。用荧光金和NADPH-黄递酶组织化学进行双重标记显示,再生的CN神经元不表达一氧化氮合酶(NOS)。我们的结果表明,CS对脊髓损伤后CN神经元的再生具有抑制作用。