NgR在中菊头蝠(Rhinolophus affinis)脑中分布

Nogo和其受体相互作用可能在抑制神经再生中发挥着重要作用.运用免疫细胞化学方法,本研究观察了Nogo受体(NgR)在中菊头蝠脑中的分布.结果显示NgR在中菊头蝠脑皮层各层均有表达.在海马,NgR主要分布在CA1、CA3和DG区的神经细胞胞膜、胞质或/和突起上.杏仁核、丘脑、室旁核、视上核、视交叉上核等也有NgR阳性神经细胞着色.在脑的白质,轴突着色明显.小脑的分子层、Purkinje细胞层和颗粒细胞层均有NgR免疫阳性反应,其中阳性反应的颗粒细胞最多.这些提示NgR可能介导其配基对中菊头蝠脑多个区域的神经细胞起作用.     

中枢髓鞘源性抑制蛋白与中枢神经再生

Nogo是一类中枢髓鞘源性抑制蛋白,主要由少突胶质细胞表达,是抑制中枢神经元轴突再生的抑制因子。这些研究成果为探讨CNS损伤的治疗提供了新思路。论文综述了Nogo的结构及在CNS中对神经元轴突再生的抑制作用。     

Myelination in the hippocampus during development and following lesion

Myelin is crucial for the stabilization of axonal projections in the developing and adult mammalian brain. However, myelin components also act as a non-permissive and repellent substrate for outgrowing axons. Therefore, one major factor which accounts for the lack of axonal regeneration in the mature brain is myelin. Here we report on the appearance of mature, fully myelinated axons during hippocampal development and following entorhinal lesion with the myelin-specific marker Black Gold. Although entorhinal axons enter the hippocampal formation at embryonic day 17, light and ultrastructural analysis revealed that mature myelinated fibers in the hippocampus occur in the second postnatal week. During postnatal development, increasing numbers of myelinated fibers appear and the distribution of myelinated fibers at postnatal day 25 was similar to that found in the adult. After entorhinal cortex lesion, a specific anterograde denervation in the hippocampus takes place, accompanied by a long-lasting loss of myelin. Quantitative analysis of myelin and myelin breakdown products at different time points after lesion revealed a temporally close correlation to the degeneration and reorganization pha-ses in the hippocampus. In contrast, electroconvulsive seizures resulted in brief demyelination and a faster recovery time course. In conclusion, we could show that the appearance of mature axons in the hippocampus is temporally regulated during development. In the adult hippocampus, demyelination was found after anterograde degeneration and also following seizures, suggesting that independent types of insult lead to demyelination. Reappearing mature axons were found in the hippocampus following axonal sprouting. Therefore, our quantitative analysis of mature axons and myelination effectively reflects the readjusted axonal density and possible electrophysiological balance following lesion. Received 22 December 2003; received after revision 11 February 2004; accepted 17 February 2004