神经节苷脂GM_1在周围神经系统中的研究

神经节苷脂GM1（ganglioside，GM1）最早被认为主要存在于中枢神经，尤其以脑中含量最丰富。而自Macmilla[1]等人证明坐骨神经、股神经中也含有GM1以来，GMI和抗GMI抗体在周围神经中的作用越来越引起人们的重视。目前的初步研究已从不同程度、不同侧面揭示了GM1和抗GM1抗体与周围神经系统疾病有密切关系。一、GM1和抗GM1抗体神经节着脂是神经系统糖脂的主要组成部分，其化学成份为含唾液酸的寡糖链和神经酸胺。分为单唾液酸神经节着脂（GM1、GM2、GM3），双唾液酸神经节音脂（GD1a、GD1b），三唾液酸神经节苷脂（GQ1b。研究发…     

神经节苷脂在中枢神经系统创伤中应用的研究

神经节苷脂(Ganglioside,Gg)是一种由带有唾液酸的寡糖链和神经酰胺组成的糖鞘脂,是大多数哺乳动物细胞膜双脂层(包括神经细胞突触终板、高尔基体膜、内质网膜和洛酶体膜等生物膜)的组成成分。在神经系统特别是大脑皮质中尤为丰富。外源性Gg可以通过血脑屏障嵌入神经细胞膜,参与神经元的生长、分化和再生过程。     

神经节苷脂对缺血性大鼠脑损伤作用的研究

目的 探讨神经节苷脂（ＧＭ１）的脑保护作用及其可能机制。方法 用四血管闭塞４ＶＯ）全脑缺血再灌注模型,用高效液相色谱仪柱前衍生色谱法测定假手术组,缺血３０ｍｉｎ再灌注６０ｍｉｎ生理盐水（ＮＳ）处理组、缺血３０ｍｉｎ再灌注６０ｍｉｎＧＭ１处理组的海马组织兴奋性氨基酸（ＥＡＡ）含量,并观察缺血３０ｍｉｎ再灌注４ｄ海马ＣＡ１区病理变化。结果 缺血再灌注ＮＳ处理组海马组ＥＡＡ含量显著性降低,海马ＣＡ１区多     

神经节苷脂对大鼠脑缺血的早期保护作用

本文以皮层脑电图为观察指标，探讨神经节苷脂对大脑中动脉阻断１２小时后引起脑缺血的早期保护作用。采用Ｓ·Ｔ·Ｃｈｅｎ等的方法制备脑缺血模型。术后腹腔注射神经节苷脂。脑缺血１２小时记录三区域皮层电图（额、中央、顶区），以频率和波幅功率谱的积分值，对组间、左、右皮层相应各区比率进行统计学处理。实验结果表明，脑缺血组各区比率均较假手术组明显降低，差异显著（ｐ＜０．０１）。神经节苷脂组各区比率均高于脑缺血组，差异显著（ｐ＜０．０１）。提示：神经节苷脂对脑缺血引起的脑电改变具有早期保护作用。     

神经节苷脂治疗出血性脑梗死疗效评价

2009-06-2011-06我院应用神经节苷脂治疗出血性脑梗死（HI）患者80例,取得良好疗效,现报告如下。1资料与方法1.1一般资料选择在中国人民解放军第150中心医院神经内科住院治疗的160例出血性脑梗死患者,经头颅CT或MRI检查证实。将160例患者随机分为治疗组和对照组,治疗组80例,男58例,女32例;平均年龄60岁;     

神经生长因子和神经节苷脂的研究进展

1 神经生长因子1.1 神经生长因子的生理作用 NGF最初是从小鼠的颌下腺提取的,许多组织和细胞在人工培养的条件下也可以产生低水平的NGF.其分子量140000左右,有三个亚单位组成(α、β、γ).     

神经节苷脂治疗急性脑梗死的疗效观察

目的观察神经节苷脂(GM1)治疗急性脑梗死的疗效。方法将60例急性脑梗死患者随机分为GM1组和对照组,在同时给予常规治疗的基础上,分别采用GM1 40 mg或胞二磷胆碱0.75 g加入250 m l生理盐水中静脉滴注,每日1次,共2周;观察两组患者治疗前后神经功能缺损程度评分(NDS)及日常生活活动量表(ADL)评分的变化及不良反应。结果治疗后GM1组及对照组NDS及ADL评分与治疗前相比均有显著改善(P<0.05~0.01);GM1组改善程度与对照组相比差异有极显著性(均P<0.01)。两组均未发现明显不良反应。结论GM1治疗急性脑梗死疗效显著。     

神经节苷脂治疗急性脑梗死的疗效观察

目的 探讨神经节苷脂治疗急性脑梗死的临床疗效.方法 将60例急性脑梗死患者随机分为观察组和对照组各30例,2组均给予常规治疗的基础上,对照组给予胞二磷胆碱治疗,观察组给予神经节苷脂治疗.结果 观察组总有效率100%,对照组总有效率60%,观察组疗效优于对照组,2组比较差异具有统计学意义 (P<0.05).结论 神经节苷脂治疗急性脑梗死疗效显著,且安全性好,值得临床推广应用.     

神经节苷脂治疗急性脑梗死的疗效观察

目的观察神经节苷脂（GM1）对急性脑梗死的治疗效果。方法急性脑梗死患者78例,随机分为治疗组38例,GM132mg加入250ml生理盐水中静滴,1次／d,2周为一疗程;对照组40例,基础药物治疗。治疗组除加用GM1外,两组治疗基本相同。于治疗前、后对两组病人的神经功能缺损程度（NDS）及日常生活活动量（ADL）进行评分比较。结果治疗组在治疗前、后比较NDS评分及ADL评分有显著差异（P〈0．01）;治疗组与对照组相比,NDS评分和ADL评分有显著差异（P〈0．05）。结论GM1能改善急性脑梗死病人的预后,降低病人的神经功能的缺损程度。     

单唾液酸四己糖神经节苷脂钠治疗糖尿病周围神经病变临床疗效观察

目的探讨单唾液酸四己糖神经节苷脂钠(GM1)治疗糖尿病周围神经病变临床应用前景。方法将56例糖尿病周围神经病变患者随机分为GM1治疗组和甲钴胺治疗组,两组均给予常规降糖、改善循环等治疗,3个月后观察治疗前后临床症状改善情况并测定治疗前后患者血清一氧化氮(NO)水平。结果①GM1组治疗有效率高于甲钴胺组,但差异无统计学意义,(P>0.05);②治疗前两组NO水平差异无统计学意义,治疗后两组自身比较,差异有统计学意义(P<0.001),且治疗后GM1组明显高于甲钴胺组(P<0.001)。结论 GM1治疗糖尿病周围神经病变有良好前景,待进一步观察。     

Sympathetic nerve fibers in peripheral sensory and motor nerves in the face of the rat

Retrograde transport of horseradish peroxidase (HRP) has been used to investigate whether postganglionic neurons in the superior cervical ganglion send branches into various peripheral nerves in the rat. HRP was applied to the zygomatic branch of the facial nerve, the mental nerve, deep vibrissae nerves and to nerves in the tooth pulp. HRP-labeled neurons were consistently seen in the SCG in all types of experiments, except for the cases where HRP was applied to the tooth pulp.     

Differential atrophy of sensory and motor fibers following section of cat peripheral nerves

Differential effects of peripheral nerve section on myelinated sensory and motor fiber populations were investigated in 5 hindlimb nerves of cats. Upon electrical stimulation of each nerve, monophasic compound action potentials were recorded from the L6, L7 and S1 dorsal and ventral roots, and the impedance of each root was measured. The decline in the electrical charge computed from potentials 43 to 252 days after nerve section gave a measure of the effect of axotomy on the diameters of sensory and of motor fibers in each nerve. No significant difference in the rate of atrophy of sensory and motor fibers was observed after about 45 days following nerve section. After about 145 and 245 days, however, dorsal root charge contributions had decreased significantly more than ventral root values. Exponential decay curves were fitted separately to charge data for sensory and for motor fibers. The calculated value for the endpoint of the decay was about 35% of the control value for motor fibers, and not significantly different from zero to sensory fibers. These results suggest that in response to axotomy, myelinated motor fiber diameters decline at first but later stabilize, while myelinated sensory fibers continue to decline and may atrophy completely if regeneration is prevented. Possible roles of electrical activity and of 'trophic' interactions with the periphery in the maintenance of cell properties are discussed.     

Immunohistochemical study on the distribution of neuron-specific enolase- and peptide-containing nerves in the omasum of cattle

The distribution of nerves containing immunoreactivity for substance P (SP), vasoactive intestinal polypeptide (VIP), leucine-enkephalin (LENK), and gastrin-releasing polypeptide (GRP) in the margin of the reticulo-omasal orifice, omasum, and omasal pillar of calves and cows was studied by immunohistochemistry. The general distribution of nerves was determined by means of neuron-specific enolase (NSE) antiserum and then compared to the distribution of immunoreactive (IR) nerves stained for the four peptides. Marked differences in the distribution of immunoreactive nerves were associated with age and the segment examined. SP-IR fibers were abundant in the musculature of the ungulate papillae at the reticulo-omasal orifice and in the smooth muscle of the omasal leaves, moderately dense in the omasal pillar, and low in density in the inner muscle layer of the reticulo-omasal orifice and in the muscle of the omasal wall. In order of decreasing abundance, the cell bodies of SP-IR nerves were found at the reticulo-omasal orifice, in the omasal wall, and in the omasal pillar. LENK-IR fibers, though less abundant, showed a pattern of distribution that was similar to that of SP-IR fibers. Nerve cell bodies showing weak immunoreactivity for LENK were detected rarely. Abundant VIP-IR fibers were present in the inner muscle layer of the reticulo-omasal orifice and in the omasal wall, while moderate numbers were seen in the omasal pillar: they were low in density in the ungulate papillae and omasal leaves. Cell bodies of VIP-IR nerves decreased in number through the omasum, reticulo-omasal orifice, and omasal pillar. The distribution of GRP-IR nerve fibers was similar to that of VIP-IR fibers, although GRP-IR fibers were less abundant. Nerve cell bodies showing weak immunoreactivity for GRP were detected rarely. The individual distribution of peptide-IR nerves was similar in the calf and cow, but immunoreactive nerves were far more abundant in the calf. The present study provides valuable information for discussion of the possible role of nerves in the regulation of omasal function.     

The effects of age and ganglioside composition on the rate of motor nerve terminal regeneration following antibody-mediated injury in mice

Gangliosides are glycosphingolipids highly enriched in neural plasma membranes, where they mediate a diverse range of functions and can act as targets for auto-antibodies present in human immune-mediated neuropathy sera. The ensuing autoimmune injury results in axonal and motor nerve terminal (mNT) degeneration. Both aging and ganglioside-deficiency have been linked to impaired axonal regeneration. To assess the effects of age and ganglioside expression on mNT regeneration in an autoimmune injury paradigm, anti-ganglioside antibodies and complement were applied to young adult and aged mice wildtype (WT) mice, mice deficient in either b- and c-series (GD3sKO) or mice deficient in all complex gangliosides (GM2sKO). The extent of mNT injury and regeneration was assessed immediately or after 5 days, respectively. Depending on ganglioside expression and antibody-specificity, either a selective mNT injury or a combined injury of mNTs and neuromuscular glial cells was elicited. Immediately after induction of the injury, between 1.5% and 11.8% of neuromuscular junctions (NMJs) in the young adult groups exhibited healthy mNTs. Five days later, most NMJs, regardless of age and strain, had recovered their mNTs. No significant differences could be observed between young and aged WT and GM2sKO mice; aged GD3sKO showed a mildly impaired rate of mNT regeneration when compared with their younger counterparts. Comparable rates were observed between all strains in the young and the aged mice. In summary, the rate of mNT regeneration following anti-ganglioside antibody and complement-mediated injury does not differ majorly between young adult and aged mice irrespective of the expression of particular gangliosides. Synapse 67:382–389, 2013. © 2013 Wiley Periodicals, Inc.     

Functional and morphological effects of repeated sodium arsenite exposure on rat peripheral sensory nerves

Exposure to inorganic arsenic (iAs) is known to result in peripheral neuropathy. To better understand the functional and morphological consequences of iAs exposure, we examined the electrophysiological and histological characteristics of the sensory sural nerves in adult Male Wistar rats following 30 days of sodium arsenite administration by gavage (10 mg/kg body weight/day). Arsenic (As) levels in the peripheral nerves of exposed animals were about 150 times greater than those in controls. Lipid peroxidation was also increased in iAs-exposed animals. Compound action potentials (CAPs) evoked in iAs-exposed nerves were characterized by a slower conduction velocity ( approximately 26%). iAs-exposed nerves also showed a trend towards a decreased CAP area ( approximately 35%). These electrophysiological changes were consistent with histological alterations such as a approximately 56% decrease in myelin thickness. In addition, the perimeter and transverse area of axons were reduced to 29% and 45% of control, respectively. Our results suggest that accumulation of As produced by iAs exposure induces oxidative damage, severe demyelination, and other morphological alterations in axons of peripheral nerves. These changes may, in turn, induce changes in the generation and propagation of action potentials in peripheral nerves, leading to decreased transmission of information from peripheral sensory organs to the central nervous system.     

Experimental alcoholic neuropathy in the rat: Histological and electrophysiological study on the myoneural junctions and the peripheral nerves

Summary Peripheral nerves and myoneural junctions of the tibialis anterior muscle of the rat were studied histologically and electrophysiologically after various periods of peroral ethanol treatment. Histochemical distributions of non-specific cholinesterase (ns. ChE; E.C. 3.1.1.8) and acetylcholinesterase (AChE; E.C. 3.1.1.7) activity of the muscle were normal during the first 3 months of daily ethanol drinking. After 5 months of exposure to 10–25% (v/v) ethanol as the sole drinking fluid, pathological ns. ChE activity was seen sporadically along the intramuscular nerves with slight ultrastructural changes in the Schwann cells. After 7 months of ethanol treatment there was further increased pathological ns. ChE activity in the intramuscular nerves while the AChE activity remained normal in the muscle. More prominent ultrastructural changes were seen in the Schwann cells namely swelling and vacuolization of the cytoplasm and dilatation of the rough endoplasmic reticulum. Increased numbers of small axons were also seen. After 9.5 months on alcohol marked increase in the ns. ChE activity was observed along most of the intramuscular nerves. AChE activity of the myoneural junctions was only sporadically weakened.A slight slow-down in the conduction velocity of the large myelinated size A fibers was observed in the animals on alcohol from 7–9.5 months, whereas the conduction velocity of the smaller myelinated B fibers was not appreciably changed. The present experiment indicates that progressive neuropathy can be induced in rats by oral alcohol feeding along with the normal laboratory diet. The first pathological changes were seen in the Schwann cells and could well be followed by the methods employed. The present experimental model can possibly be used in future studies concerning the development of toxic polyneuropathy.Supported by the Finnish Foundation for Alcohol Studies     

Basic and clinical aspects of autoimmune disorders in peripheral nerves

This presentation discusses the immunobiology of the Guillain Barré syndromes (GBS), the world's leading cause of acute autoimmune neuromuscular paralysis. By gaining an understanding of the clinical and pathophysiological pathways operating in GBS, we can hope to develop novel immunotherapies that will improve clinical outcome. Here we focus on GBS mediated by anti-ganglioside antibodies and highlight the correlations between anti-ganglioside antibody patterns and clinical phenotypes, the development of models of GBS, and the application of novel therapies based on inhibition of complement activation.     

Quantitative studies of the abnormal axon-Schwann cell relationship in the peripheral motor and sensory nerves of the dystrophic mouse

The nature and extent of abnormal axon-Schwann cell relationships in peripheral portions of dystrophic motor and sensory nerves were quantitatively evaluated between 1 and 9 months of age using teased fibres and electron micrographs.The results show that in the dystrophic (dy/dy) common peroneal (CPN) and tibial nerves (TN), and less in the dy/dy sural nerve (SN): (1) the number of Schwann cell nuclei associated with myelinated axons is increased with respect to normal; (2) the average internodal length is correspondingly reduced; (3) the average dystrophic internode elongates roughly in parallel with the average normal internode, and with the dystrophic limb; the longitudinal growth of the dystrophic limb is normal; (4) the variation of internodal length is greater than normal; it does not increase with age; (5) the incidence of the nodes of Ranvier which are wider than the normal 3 μm limit does not increase with age; and (6) the number of myelinated axons is reduced in the dy/dy CPN and TN but not in the dy/dy SN; it shows no change with age.These data indicate that: (1) in the dy/dy peripheral nerves (PNS) the abnormal axon-Schwann cell relationships and the reduced number of myelinated axons have been established prior to 1 month of age, thereafter progressive degenerative processes do not appear to take place, and (2) the dy/dy sensory nerve are less affected than the motor ones.