DO ASTROCYTES AFFECT THE SYMPTOMS OF MULTIPLE SCLEROSIS

一种新的中枢性脱髓鞘病变分类及其标记方法 钠通道分布沿着神经，将被应用于 中枢神经病变的形态学和生理学检查。 具体来说，该项目将研究神经胶质细胞的潜在作用， 细胞（星形胶质细胞和少突胶质细胞）在影响生理 病理性中枢神经纤维的性质。 香港会继续担当这个角色 通过比较五种因素之一对纤维性能的影响， 脱髓鞘病变的分类。 每类病变将 其特征在于不同类型的神经胶质存在：即1） 慢性神经胶质细胞无脱髓鞘神经纤维（在此介绍） 应用见图1）; 2）慢性神经胶质细胞相关的损伤 脱髓鞘神经纤维（中枢白喉毒素损伤）; 3）a 无神经胶质细胞的稳定病变，神经胶质细胞随后 4）胶质相关纤维的稳定病变，其中胶质细胞 细胞随后被移除;以及5）其中脱髓鞘纤维 经历髓鞘再生（中枢溶血性损伤）。 这些病变 将进行形态学和电生理学检查。 形态学上，病变将被检查，以确定钠 沿着脱髓鞘的轴膜分布，这种分布 将与周围的神经胶质细胞（当存在时）进行比较。 钠通道将使用本研究中介绍的一种新技术进行标记。 应用程序（见图2）。 从生理学上讲，不同的病变 检查：1）是否存在通过病变的传导; 2)（3）安全性;（4）安全性;（5）安全性。 纤维异位产生动作电位。 这些生理 这些特性被认为决定了 瘫痪和失明等阴性症状，以及 阳性症状如感觉异常。 通过比较获得的结果， 通过对不同病变的研究，神经胶质细胞对 脱髓鞘的轴突应该被揭示出来，它们对神经元的贡献也应该被揭示出来。 对脱髓鞘疾病的神经病学认识更加清楚。 在 例如，多发性硬化症的病变， 星形胶质细胞与不同脱髓鞘轴突的结合程度， 考虑到星形胶质细胞的特性， 这种变化可能导致在生理特性上的差异 轴突 例如，星形胶质细胞的有效性可能 响应可以确定缓解的存在或不存在。 当然， 希望更好地理解 神经胶质细胞在病理过程和修复可能导致新的 多发性硬化症及相关疾病的对症治疗方法 紊乱

A new class of central demyelinating lesion, and a new method of marking the sodium channel distribution along nerves, will be applied to a morphological and physiological examination of central neuropathy. Specifically, the project will examine the potential role of neuro-glial cells (astrocytes and oligodendrocytes) in influencing the physiological properties of pathological central nerve fibres. This role will be investigated by comparing the properties of fibers affected by one of five classes of demyelinating lesion. Each class of lesion will be characterised by a different type of glial presence: namely 1) a lesion of chroncially glial cell-free demyelinated nerve fibers (introduced in this application see figure 1); 2) a lesion of chronically glial cell-associated demyelinated nerve fibers (the central diphtheria toxin lesion); 3) a stable lesion free of glial cells to which glial cells are later introduced; 4) a stable lesion of glial-associated fibers from which glial cells are later removed; and 5) a lesion in which the demyelinated fibers undergo remyelination (the central lysolecithin lesion). These lesions will be examined both morphologically and electrophysiologically. Morphologically, the lesions will be examined to determine the sodium channel distribution along the demyelinated axolemma, and this distribution will be compared with that of the surrounding glial cells (when present). The sodium channels will be marked using a new technique introduced in this application (see figure 2). Physiologically, the different lesions will be examined for: 1) the presence or absence of conduction through the lesion; 2) the security of the conduction when present; and 3) the ability of the fibers to generate action potentials ectopically. These physiological properties are believed to determine both the presence or absence of negative symptoms such as paralysis and blindness, and the generation of positive symptoms such as paraesthesiae. By comparing the results obtained from study of the different lesions the potential effects of glial cells on demyelinated axons should be revealed, and their contribution to the symptomatology of demyelinating disease more clearly understood. In the lesion of multiple sclerosis for example, there is a marked variation in the degree of association of astrocytes to different demyelinated axons, and considering the properties of astrocytes it is pertinent to question if this variation may cause differences in the physiological properties of the axons. It is for example possible that the effectiveness of the astrocyte response may determine the presence or absence of remissions. Certainly, it is not unreasonable to hope that a greater understanding of the role of neuro-glial cells in pathological processes and repair may lead to new approaches in the symptomatic therapy of multiple sclerosis and related disorders.