OECs移植联合IN-1抗体修复急性脊髓损伤的实验研究

目的研究嗅鞘细胞移植联合轴突生长抑制蛋白抗体IN-1局部持续注射对大鼠横断性脊髓损伤的修复作用.方法成年雄性SD大鼠40只,建立胸脊髓全横断损伤模型,随机分成单纯对照组(10只)、嗅鞘细胞移植组(10只)、IN-1抗体微泵注射组(10只)和嗅鞘细胞移植联合IN-1抗体组(10只).应用NF200免疫组化染色和免疫荧光染色对脊髓损伤区神经纤维再生进行形态学观察.采用BBB评分评估大鼠后肢功能恢复情况.结果横断损伤共有9只大鼠死亡.术后8周可观察到Hoeehet标记的嗅鞘细胞在体内存活并在脊髓内迁移;联合治疗(OECs IN-1)组和OECs组可见脊髓损伤区杂乱无序的再生轴突,但无连续性神经纤维通过损伤区;IN-1组和对照组脊髓残端萎缩,未见轴突再生.后肢功能运动平均BBB评分对照组、IN-1抗体组、细胞移植组和联合治疗组分别为7.70±0.24、7.89±0.15、10.50±0.25、11.33±0.24.结论OECs移植联合IN-1抗体可促进损伤的脊髓神经轴突的存活和再生,较单纯应用OECs或IN-1能更好的促进脊髓损伤修复和大鼠后肢功能恢复.     

脊髓全横断模型大鼠的行为学与病理学对照（英文）

背景:理想的脊髓损伤模型应既能模拟人类脊髓损伤,又能排除影响疗效的干扰因素,并具有广泛可重复性,脊髓全横断模型是目前较理想的选择。但由于操作方法的多样性致使疗效差异较大,各研究结果之间缺乏可比较性。目的:通过建立标准化的大鼠脊髓全横断模型,对比分析脊髓全横断大鼠后肢行为学改变和病理学特征。方法:成年雌性SD大鼠60只,随机分为假手术组(n=12)、常规脊髓横断组(n=24)和显微脊髓横断组(n=24),每组再随机分为造模后7,14,28 d组。以T9椎体为中心,假手术组行椎板切除;其他两组行脊髓全横断,造成脊髓急性损伤模型,其中常规脊髓横断组采用常规外科方法造模,显微脊髓横断组采用标准化显微操作技术造模。各组于造模后7,14和28 d行后肢运动功能BBB评分及横断处脊髓的组织病理学观察,观测脊髓横断处瘢痕组织厚度、脊髓残端间距、空洞横径和脑脊液囊腔形成情况,计算瘢痕指数、残端间距指数和空洞指数。结果与结论:假手术组术前、术后BBB评分和脊髓病理无明显变化。常规脊髓横断组和显微脊髓横断组大鼠造模后后肢完全性瘫痪,其中常规脊髓横断组大鼠后肢功能无恢复。造模后一至二周,显微脊髓横断组大鼠开始出现后肢运动功能自发性恢复,脊髓病理学检测指标值均明显低于常规脊髓横断组,差异有非常显著性意义(P0.01)。各组病理学观测指标与BBB评分之间无相关关系。提示标准化脊髓全横断造模方法有利于消除个体差异,更有利于对治疗效果的量化分析和研究比较。     

大鼠脊髓横断伤后护理对生存质量及功能评分的影响

目的通过脊髓损伤(SCI)后的科学护理,探讨提高动物的生存率及生存质量的方法。方法制作SCI动物模型,分为A、B两组,脊髓横断伤不作护理为A组(非护理组),脊髓横断伤行术后护理为B组(护理组)。观察两组动物的生存率、生存质量及行为学评分(BBB),并进行比较。结果脊髓损伤护理组的生存率及生存质量与脊髓损伤非护理组比较,具有显著性差异(P<0.05),护理组高于非护理组。结论脊髓横断伤模型护理可提高动物生存率,改善生存质量,有助于提高实验动物的样本量。     

不同脊髓损伤模型大鼠行为学及形态学的变化

背景：在脊髓全断模型中有切割伤模型、切除伤模型,为了更好地选择脊髓损伤修复研究的全断动物模型,有必要对这两种模型进行比较及探讨。 目的：分析不同脊髓损伤模型的行为学及病理变化,选择适用于再生研究及治疗的脊髓损伤动物模型。 方法：将160只SD大鼠随机均分为2组,分别制作切割型脊髓损伤模型与切除型脊髓损伤模型,术后1,2,4,8,10,20,30,50周内进行后肢行为学BBB评分及组织化学、免疫组织化学染色,观察损伤区残余纤维情况;术后4,10,26,52周分别在大鼠脑皮质运动区与颈髓注射BDA-FITC示踪剂,观察损伤区残余纤维的连续性。 结果与结论：切割脊髓损伤模型组大鼠术后2-50周双后肢的BBB得分明显高于切除脊髓损伤模型组(P < 0.05);切割脊髓损伤模型组在损伤区残存大量组织和神经丝、胶质纤维酸性蛋白纤维,而切除脊髓损伤模型几乎没有残存纤维;不论是切割脊髓损伤模型还是切除脊髓损伤模型,皮质脊髓束均不能通过损伤区,终止于损伤区的头端;在切割脊髓损伤模型中,脊髓固有束重新进入尾侧端的宿主脊髓组织中,而在切除脊髓损伤模型中脊髓固有束终止于损伤区的头端。表明切除脊髓损伤模型更适用于脊髓损伤后再生效果及治疗手段或药物的筛选与评价。 中国组织工程研究杂志出版内容重点：肾移植;肝移植;移植;心脏移植;组织移植;皮肤移植;皮瓣移植;血管移植;器官移植;组织工程      

A型肉毒杆菌神经毒素重链干预大鼠脊髓损伤后蛋白表达的初步研究

目的:初步观察大鼠脊髓损伤模型基础上局部注射小剂量A型肉毒杆菌神经毒素重链(BoNT/A HC)后对局部蛋白表达谱的影响,为探讨BoNT/A HC干预在体神经损伤后相关蛋白表达及其干预神经再生机制提供实验基础。方法:复制大鼠单侧腰段脊髓损伤模型;采用SDS-PAGE及双向电泳观察不同剂量BoNT/A HC(2μg、4μg、6μg和8μg)对脊髓损伤后局部(包括损伤部位及其近头端部分脊髓组织)蛋白表达谱的干预作用。结果:大鼠单侧腰段脊髓损伤2 d时局部脊髓组织结构明显破坏崩解,损伤波及左侧脊髓灰质及白质;脊髓损伤局部SDS-PAGE及考马斯亮蓝染色显示,于损伤同时局部一次性注射不同剂量BoNT/A HC后,某些蛋白表达与单纯损伤组相比明显不同,而与正常组基本一致;双向电泳结果进一步显示,损伤局部注射6μg BoNT/A HC后2 d和20 d时,在不同等电点及不同蛋白分子量水平上,有10余种蛋白表达与单纯损伤组明显不同,呈向正常转化的趋势。结论:大鼠脊髓损伤局部注射BoNT/A HC一定时间可影响损伤局部蛋白表达谱的变化,这种变化呈现由损伤造成的蛋白表达变化被转向正常的趋势。     

大鼠脊髓损伤后局部应用聚乙二醇的抗神经纤维溃变研究

目的:探讨大鼠脊髓损伤后局部应用聚乙二醇(polyethylene glycol,PEG)的抗神经纤维溃变作用。方法:选取健康雄性Wistar大鼠,所有动物随机分为对照组和PEG治疗组。各组动物制作脊髓横断损伤模型。PEG治疗组大鼠在脊髓横断后,蛛网膜下腔立即注射PEG。对照组大鼠用生理盐水代替PEG,其余步骤相同。各组大鼠存活1、2、3 d后处死取材。标本切片后分别进行Massons染色和免疫荧光染色,比较各组切片每个高倍视野内的神经纤维溃变轴索球数目。其余动物麻醉后取出新鲜脊髓标本,制成匀浆后用免疫印迹法测定脊髓组织内钙蛋白酶(m-calpain)和神经丝蛋白(neurofilement,NF-200)降解产物的相对含量。结果:(1)对照组脊髓损伤部位大量炎症细胞浸润,组织坏死严重,损伤近侧端的轴索球明显多于PEG治疗组;PEG治疗组炎症反应较轻,组织坏死不明显,轴索球数目少于对照组。(2)PEG治疗组脊髓组织内m-calpain以及NF降解产物的含量均显著低于对照组。结论:大鼠脊髓损伤早期局部应用PEG可以有效减轻神经纤维的溃变。     

建立脊髓横断模型大鼠的系统评价

背景：建立一种成功率较高、安全可靠的标准脊髓横断模型是研究脊髓修复的前提条件。目的：评价大鼠脊髓横断模型制备的价值及椎板切除对脊髓的影响。方法：检索美国国立医学图书馆(PubMed)、中国知网(CNKI)、重庆维普(VIP)、万方数据库中所用关于大鼠脊髓横断模型的随机对照研究。结果与结论：11篇随机对照研究符合纳入标准(英文2篇,中文9篇),共394只大鼠纳入研究,脊髓半横断组与椎板切除组1-6周内下肢运动功能评分(BBB评分)、4周内电生理差异有显著性意义(WMD=-12.86,95%CI-16.10至-9.62,P < 0.01)、(WMD=15.36,95%CI 11.36-19.36,P < 0.01),半横断组6周后BBB评分差异无显著性意义(WMD=-10.28;95%CI -24.20-3.64;P=0.15);脊髓全横断组与椎板切除组1-6周内BBB评分、4周内电生理差异有显著性意义(WMD=-18.83,95%CI -20.64至-17.01,P < 0.01)、(WMD= -11.21,95%CI -16.35至-6.08,P < 0.01)。椎板切除组与正常组4周内BBB评分与电生理评分差异无显著性意义(WMD=-0.00,95%CI -0.01-0.01,P=1)、(WMD= 0.43,95%CI -0.35-1.21,P=0.28);大鼠脊髓横断组和椎板切除组死亡数差异无显著性意义(RD=0.05,95%CI -0.03-0.13;P=0.26)。说明脊髓横断法是一种稳定性好、可复制性强、存活率高的脊髓损伤研究模型,但其横断的准确性、术后护理及对照组的设立有待商榷。中国组织工程研究杂志出版内容重点：肾移植;肝移植;移植;心脏移植;组织移植;皮肤移植;皮瓣移植;血管移植;器官移植;组织工程     

两种督脉电针对大鼠脊髓受损伤神经元存活的影响

目的探讨脊髓损伤区近端督脉2个穴位电针和脊髓损伤区远、近端督脉4个穴位电针对全横断脊髓损伤大鼠腰段脊髓神经元存活与凋亡的影响。方法雌性SD大鼠30只,随机分为对照组、近端督脉穴电针组(EA2组)和远近端督脉穴电针组(EA4组),每组10只大鼠,其中每组各5只分别应用于免疫荧光染色和Western blot检测。在所有大鼠脊髓第10胸段(T10)进行全横断损伤手术。EA2组在脊中(GV9)和至阳(GV6)督脉穴位入针,EA4组在GV9、GV6、腰腧(GV4)和长强(GV1)督脉穴位入针。在术后第3 d开始电针,隔天1次,每次20 min。术后14d后将3组动物取材进行后续实验。Western blot检测脊髓组织活化型半胱天冬酶-3的表达情况。结果与对照组和EA 2组相比,EA 4组可增加脊髓腰段神经元存活数量、减少脊髓腰段神经元凋亡率和下调脊髓腰段组织表达活化型半胱天冬酶-3(P<0.05)。结论脊髓损伤区远近端督脉4个穴位电针要比脊髓损伤区近端督脉2个穴位电针更有效地促进受损伤脊髓腰段神经元存活和减少其凋亡,下调受损伤脊髓腰段组织表达凋亡相关蛋白。     

针刺对脊髓全横断SD大鼠BDNF基因表达的影响

目的探讨电针刺对脊髓全横断成年SD大鼠脑源性神经营养因子(brain-derived neurotrophic fac-tor,BDNF)mRNA在横断脊髓上端、下端、大脑皮质和比目鱼肌中的表达及变化的影响。方法建立40只SD大鼠脊髓全横断损伤模型,雌雄不限,随机分为针刺1d、3d、7d、14d和手术1d、3d、7d、14d组,每组5只,选"足三里 悬钟"及"三阴交 伏兔"2组穴位隔天交替针刺。采用RT-PCR技术检测各时间段脊髓横断上、下端、大脑皮质、比目鱼肌四部位中BDNF mRNA的表达。结果针刺14d组比目鱼肌中BDNF mRNA较手术14d组显著增加(P<0.05)。结论电针刺可促进BDNF在损伤部位所支配的肌肉-靶组织中的表达。     

督脉电针对早期受损伤的脊髓神经营养素-3表达的影响

目的 观察督脉电针对早期受损伤的脊髓神经营养素-3(NT-3)表达的影响及其细胞定位.方法 成年雌性大鼠分为损伤组和电针加损伤组.全横断损伤两组大鼠的脊髓1d后,开始对电针+损伤组大鼠进行督脉电针,损伤组大鼠不做督脉电针.电针加损伤组在电针后1、3和7d时间点取出脊髓损伤区组织,损伤组也在相应时间点取出损伤区组织,用ELISA方法检测损伤区组织NT-3水平.再取电针后7d大鼠脊髓损伤区及其邻近组织切片做NT-3的免疫荧光组织化学双标染色.结果 电针加损伤组和损伤组的脊髓损伤区组织NT-3表达在时间上基本一致;在前3 d,NT-3水平是下降的,在后3 d,NT-3水平是增高的.但是,与损伤组相比,电针加损伤组的NT-3水平是明显增高(P＜0.05).免疫荧光双标染色结果显示,神经元、星形胶质细胞、少突胶质细胞和巨噬细胞都有NT-3的表达.结论 督脉电针可以促进受损伤早期的脊髓组织细胞合成和分泌内源性NT-3,这可能是督脉电针促进急性脊髓损伤修复的适宜微环境因素之一.     

Motoneuron response to dorsal root stimulation in anesthetized monkeys after spinal cord transection

Summary In preparation for studying the spinal cord alterations produced by operant conditioning of spinal reflexes, we studied peripheral nerve responses to supramaximal dorsal root stimulation in the lumbosacral cord of deeply anesthetized monkeys before and after thoracic cord transection. Except for variable depression in the first few minutes, reflex responses were not reduced or otherwise significantly affected by transection in the hour immediately following the lesion or for at least 50 h. The results suggest that reduction in muscle spindle sensitivity and/or in polysynaptic motoneuron excitation contributes to stretch reflex depression after cord transection.     

Expression of GAP-43 mRNA in the adult mammalian spinal cord under normal conditions and after different types of lesions,with special reference to motoneurons

Summary In situ hybridization histochemistry was used to detect cell bodies expressing mRNA encoding for the phosphoprotein GAP-43 in the lumbosacral spinal cord of the adult rat, cat and monkey under normal conditions and, in the cat and rat, also after different types of lesions. In the normal spinal cord, a large number of neurons throughout the spinal cord gray matter were found to express GAP-43 mRNA. All neurons, both large and small, in the motor nucleus (Rexed's lamina IX) appeared labeled, indicating that both alpha and gamma motoneurons express GAP-43 mRNA under normal conditions. After axotomy by an incision in the ventral funiculus or a transection of ventral roots or peripheral nerves, GAP-43 mRNA was clearly upregulated in axotomized motoneurons, including both alpha and gamma motoneurons. An increase in GAP-43 mRNA expression was already detectable 24 h postoperatively in lumbar motoneurons both after a transection of the sciatic nerve at knee level and after a transection of ventral roots. At this time, a stronger response was seen in the motoneurons which had been subjected to the distal sciatic nerve transection than was apparent for the more proximal ventral root lesion. An upregulation of GAP-43 mRNA could also be found in intact motoneurons located on the side contralateral to the lesion, but only after a peripheral nerve transection, indicating that the concomitant influence of dorsal root afferents may play a role in GAP-43 mRNA regulation. However, a dorsal root transection alone did not seem to have any detectable influence on the expression of GAP-43 mRNA in spinal motoneurons, while the neurons located in the superficial laminae of the dorsal horn responded with an upregulation of GAP-43 mRNA. The presence of high levels of GAP-43 in neurons has been correlated with periods of axonal growth during both development and regeneration. The role for GAP-43 in neurons under normal conditions is not clear, but it may be linked with events underlying remodelling of synaptic relationships or transmitter release. Our findings provide an anatomical substrate to support such a hypothesis in the normal spinal cord, and indicate a potential role for GAP-43 in axon regeneration of the motoneurons, since GAP-43 mRNA levels was strongly upregulated following both peripheral axotomy and axotomy within the spinal cord. The upregulation of GAP-43 mRNA found in contralateral, presumably uninjured motoneurons after peripheral nerve transection, as well as in dorsal horn neurons after a dorsal root transection, indicates that GAP-43 levels are altered not only as a direct consequence of a lesion, but also after changes in the synaptic input to the neurons.     

A mechanical microconnector system for restoration of tissue continuity and long-term drug application into the injured spinal cord

Complete transection of the spinal cord leaves a gap of several mm which fills with fibrous scar tissue. Several approaches in rodent models have used tubes, foams, matrices or tissue implants to bridge this gap. Here, we describe a mechanical microconnector system (mMS) to re-adjust the retracted spinal cord stumps. The mMS is a multi-channel system of polymethylmethacrylate (PMMA), designed to fit into the spinal cord tissue gap after transection, with an outlet tubing system to apply negative pressure to the mMS thus sucking the spinal cord stumps into the honeycomb-structured holes. The stumps adhere to the microstructure of the mMS walls and remain in the mMS after removal of the vacuum. We show that the mMS preserves tissue integrity and allows axonal regrowth at 2, 5 and 19 weeks post lesion with no adverse tissue effects like in-bleeding or cyst formation. Preliminary assessment of locomotor function in the open field suggested beneficial effects of the mMS. Additional inner micro-channels enable local substance delivery into the lesion center via an attached osmotic minipump. We suggest that the mMS is a suitable device to adapt and stabilize the injured spinal cord after surgical resection of scar tissue (e.g., for chronic patients) or traumatic injuries with large tissue and bone damages.     

Spinal cord transection modifies neuronal nitric oxide synthase expression in medullar reticular nuclei and in the spinal cord and increases parvalbumin immunopositivity in motoneurons below the site of injury in experimental rabbits

Using immunohistochemistry, we detected the expression of neuronal nitric oxide synthase (nNOS) in ventral medullary gigantocellular reticular nuclei and in the lumbosacral spinal cord 10 days after thoracic transection in experimental rabbits. We tried to determine whether neurons located below the site of injury are protected by the calcium binding protein parvalbumin (PV). Changes of nNOS immunoreactivity (IR) in spinal cord were correlated with the level of nNOS protein in dorsal and ventral horns. Ten days after transection, nNOS was upregulated predominantly in lateral gigantocellular nuclei. In the spinal cord, we revealed a significant increase of nNOS protein in the dorsal horn. This is consistent with a higher density of punctate and fiber-like immunostaining for nNOS in laminae III-IV and the up-regulation of nNOS-IR in neurons of the deep dorsal horn. After surgery, the perikarya of motoneurons remained nNOS immunonegative. Contrary to nNOS, the PV-IR was upregulated in α-motoneurons and small-sized neurons of the ventral horn. However, its expression was considerably reduced in neurons of the deep dorsal horn. The findings indicate that spinal transection affects nNOS and PV in different neuronal circuits.     

The expression of Fos-labeled spinal neurons in response to colorectal distension is enhanced after chronic spinal cord transection in the rat

The present study used Fos-like immunoreactivity to examine neuronal activation in response to colorectal distension in rats at 1 day or 30 days following spinal cord transection or sham transection. Fifty-five Wistar rats were anesthetized and an incision was made to expose the T(5) spinal segment. The dura was reflected away in all rats and a complete transection at the rostral end of the T(5) segment was given to the lesioned group. At 1 day (acute) or 30 days (chronic) post-surgery, conscious rats were subjected to a 2 h period of intermittent colorectal distension. Rats were perfused and spinal segments L(5)-S(2) were removed and processed for Fos-like immunoreactivity. Spinal cord transection alone had no effect on Fos-labeling in either acute or chronic rats. In acute rats, colorectal distension produced significant increases in Fos-labeling in the superficial and deep dorsal horn regions. In chronic rats, colorectal distension produced a three-fold increase in Fos-labeled neurons that was manifest throughout all laminar regions.These results indicate that the number of neurons expressing Fos in response to colorectal distension is much greater after a chronic spinal cord transection than after an acute transection. Since Fos is an indicator of neuronal activation, the results show that many more neurons become active in response to colorectal distension following a chronic spinal injury. This suggests that a functional reorganization of spinal circuits occurs following chronic spinal cord transection. This may ultimately result in altered visceral and somatic functions associated with spinal cord injury in humans.     

Functional recovery of stepping in rats after a complete neonatal spinal cord transection is not due to regrowth across the lesion site

Rats receiving a complete spinal cord transection (ST) at a neonatal stage spontaneously can recover significant stepping ability, whereas minimal recovery is attained in rats transected as adults. In addition, neonatally spinal cord transected rats trained to step more readily improve their locomotor ability. We hypothesized that recovery of stepping in rats receiving a complete spinal cord transection at postnatal day 5 (P5) is attributable to changes in the lumbosacral neural circuitry and not to regeneration of axons across the lesion. As expected, stepping performance measured by several kinematics parameters was significantly better in ST (at P5) trained (treadmill stepping for 8 weeks) than age-matched non-trained spinal rats. Anterograde tracing with biotinylated dextran amine showed an absence of labeling of corticospinal or rubrospinal tract axons below the transection. Retrograde tracing with Fast Blue from the spinal cord below the transection showed no labeled neurons in the somatosensory motor cortex of the hindlimb area, red nucleus, spinal vestibular nucleus, and medullary reticular nucleus. Retrograde labeling transsynaptically via injection of pseudorabies virus (Bartha) into the soleus and tibialis anterior muscles showed no labeling in the same brain nuclei. Furthermore, re-transection of the spinal cord at or rostral to the original transection did not affect stepping ability. Combined, these results clearly indicate that there was no regeneration across the lesion after a complete spinal cord transection in neonatal rats and suggest that this is an important model to understand the higher level of locomotor recovery in rats attributable to lumbosacral mechanisms after receiving a complete ST at a neonatal compared to an adult stage.     

SD大鼠脊髓损伤后微环境的模拟实验

BACKGROUND: We built Sprague-Dawley rat models with mild, moderate, and severe spinal cord injuries to accord with the spinal cord injury types for basic empirical study, and consequently to further understand the microenvironmental change in Sprague-Dawley rats with spinal cord injury, and to provide help for clinical treatment. OBJECTIVE: To observe the changes in nerve function, pathological manifestation and motor sensory evoked potential in Allen’s models and Sprague-Dawley rats with complete spinal cord transection at different time points after spinal cord injury by simulating the microenviroment in Sprague-Dawley rats. METHODS: A total of 125 healthy adult female Sprague-Dawley rats were selected and randomly divided into group sham operation group, 100 gcf hit potential group (20 g×5 cm), 200 gcf hit potential (20 g×10 cm), 300 gcf hit potential group (20 g×15 cm), and spinal cord complete transection group with 25 rats in each group. At 1, 5, 7, 14 and 28 days after model establishment, the degree of spinal cord injury was identified by the BBB scores of motion function, motor evoked potential, and pathological section. RESULTS AND CONCLUSION: (1) Totally 24 Sprague-Dawley rats died in the experiment. The death rate and the rate of complications were highest in the spinal cord complete transection group. The BBB score of each group was decreased. The BBB scores in every group increased as time went on. There were significant differences between each surgery group and the sham operation group at corresponding time points (P < 0.05).  No significant difference was found between the 300 gcf hit potential group and the spinal cord complete transection group at corresponding time points (P > 0.05). (2) In each surgery group, the infiltration of inflammatory cells and obvious swelling of neurons were visible at 1 day after injury. Neural cells reduced with time prolonged. At 28 days after injury, a large number of astrocytes proliferated, scar and spinal cord cavity formed. Above symptoms were worse in the 300 gcf hit potential group and spinal cord complete transection group than in the 100 gcf and 200 gcf hit potential groups. (3) Significant differences in amplitude and latency were detectable between each surgery group and the sham operation group (P < 0.05). No significant difference in amplitude and latency was detected between the 300 gcf hit potential group and the spinal cord complete transection group at corresponding time points (P > 0.05). Results confirmed that hit potential of 20 g×5 cm, 20 g×10 cm and 20 g×15 cm can simulate the microenvironment of Sprague-Dawley rats with mild, moderate and severe spinal cord injury. The rate of complication was lower in modified Allen’s model of different hit potentials than in models of spinal cord complete transection, and was more accorded with basic research.       

坐骨神经损伤后VIP在大鼠脊髓腰段后角中的动态变化

结扎切断SD大鼠左侧坐骨神经或前后根后,在一定的存活时间序列里,用Olympus显微镜的测光装置对经PAP法显色处理后的大鼠腰段脊髓切片后角的VIP(血管活性肠肽)进行了相对变化率(X_c/X_c-1)×100%的测定.结果发现:坐骨神经结扎切断后,术侧VIP在各个时间的值都高于对照侧;术后15天增高至125%(P<0.01),30天时仅增高至27.2%(P<0.05),120天时增高至50.7%(P<0.01)变化曲线呈双峰夹谷状.     

Retraining the injured spinal cord

The present review presents a series of concepts that may be useful in developing rehabilitative strategies to enhance recovery of posture and locomotion following spinal cord injury. First, the loss of supraspinal input results in a marked change in the functional efficacy of the remaining synapses and neurons of intraspinal and peripheral afferent (dorsal root ganglion) origin. Second, following a complete transection the lumbrosacral spinal cord can recover greater levels of motor performance if it has been exposed to the afferent and intraspinal activation patterns that are associated with standing and stepping. Third, the spinal cord can more readily reacquire the ability to stand and step following spinal cord transection with repetitive exposure to standing and stepping. Fourth, robotic assistive devices can be used to guide the kinematics of the limbs and thus expose the spinal cord to the new normal activity patterns associated with a particular motor task following spinal cord injury. In addition, such robotic assistive devices can provide immediate quantification of the limb kinematics. Fifth, the behavioural and physiological effects of spinal cord transection are reflected in adaptations in most, if not all, neurotransmitter systems in the lumbosacral spinal cord. Evidence is presented that both the GABAergic and glycinergic inhibitory systems are up-regulated following complete spinal cord transection and that step training results in some aspects of these transmitter systems being down-regulated towards control levels. These concepts and observations demonstrate that (a) the spinal cord can interpret complex afferent information and generate the appropriate motor task; and (b) motor ability can be defined to a large degree by training.     

Tissue calcium levels following spinal cord transection in rats

Adult rats were subjected to midthoracic spinal cord transections. Three segments of spinal cord, each approximately 5 mm in length, were removed from each animal at intervals from 5 min to 48 h postlesion; one from the lesion site and one each immediately rostral and caudal to the transection. Total tissue calcium concentrations ([Ca]t) for each spinal cord segment were determined using atomic absorption spectrophotometry and compared to control segments from untransected animals. [Ca]t levels in the segment at the lesion site was significantly elevated above control values at 30 min post-lesion, but decreased to control levels by 1 h. All other segments remained at control levels for the duration of the postlesion period. The rapid rise and fall of [Ca]t at the lesion site differs from spinal cord contusion studies in which [Ca]t remains at elevated levels for extended periods. It is postulated that the "open" transection injury permits the rapid clearance of calcium from the injury site.