实验性大脑皮层梗死后丘脑和纹状体突触重构与抑制性蛋白表达

目的探讨实验性大脑皮层梗死后同侧丘脑腹后外侧核和纹状体突触重构与抑制性蛋白的关系。方法采用易卒中型肾血管性高血压大鼠(RHRSP)复制右侧大脑中动脉(MCA)皮层支闭塞模型,分别于术后第1、2、3及4周,取鼠脑行免疫组化检查,检测MCA皮层支闭塞组和假手术对照组大鼠不同时点丘脑腹后外侧核和纹状体突触生长素(SYN)及胶质原纤维酸性蛋白(GFAP)、神经黏蛋白(neurocan)表达。结果MCA皮层梗死后1周,同侧丘脑腹后外侧核和纹状体SYN阳性信号较对照组高,至第2周恢复正常,第3、4周逐渐降低,且显著低于对照组。MCA皮层支闭塞后1～4周,同侧丘脑腹后外侧核和纹状体GFAP染色阳性星形胶质细胞数和Neurocan阳性信号均逐渐增多,并显著多于对照组。结论抑制性蛋白表达增加可能是脑皮层梗死后远离梗死灶的神经组织突触重构受阻的原因之一,也是梗死后神经功能恢复困难的一个重要方面。     

实验性大脑皮层梗死后丘脑和纹状体突触重构与抑制性蛋白表达

目的 探讨实验性大脑皮层梗死后同侧丘脑腹后外侧核和纹状体突触重构与抑制性蛋白的关系。方法 采用易卒中型肾血管性高血压大鼠（RHRSP）复制右侧大脑中动脉（MCA）皮层支闭塞模型，分别于术后第1、2、3及4周，取鼠脑行免疫组化检查，检测MCA皮层支闭塞组和假手术对照组大鼠不同时点丘脑腹后外侧核和纹状体突触生长素（SYN）及胶质原纤维酸性蛋白（GFAP）、神经黏蛋白（neurocan)表达。结果 MCA皮层梗死后1周，同侧丘脑腹后外侧核和纹状体SYN阳性信号较对照组高，至第2周恢复正常，第3、4周逐渐降低，且显低于对照组。MCA 皮层支闭塞后1－4周，同侧丘脑腹后外侧核和纹状体GFAP染色阳性星形胶质细胞数和Neurocan阳性信号均逐渐增多，并显多于对照组。结论 抑制性蛋白表达增加可能是脑皮层梗死后远离梗死灶的神经组织突触重构受阻的原因之一，也是梗死后神经功能恢复困难的一个重要方面。     

康复训练对脑梗塞偏瘫大鼠的行为学和脊髓GAP—43表达的影响

目的：研究康复训练对实验性脑梗塞偏瘫大鼠行为学和脊髓生长相关蛋白（GAP－43）表达的影响。方法：采用光化学法制成脑梗塞偏瘫大鼠模型,并随意分为康复训练组和制动组,每天置于滚筒式网状训练器内转动训练,在平衡木,转棒上做行走训练,共30min,每周5次,在梗后24h,7d,14d,21d,28d观察行为学变化和脊髓的GAP－43的表达,同时以正常大鼠作为对照,结果：Bederson神经功能,平衡木,转棒行走（7－28d),网屏实验（7－14d）康复组较制动组组明显好转（P＜0．05）,正常组脊髓的GAP－43较少;脑梗塞后24h康复组,制动组大鼠脊髓未瘫痪侧脊髓前角有大量的GAP－43的表达,脑通塞后7－14d康复组瘫痪侧及未瘫痪侧脊髓前角区均有GAP－43表达,制动组阳性染色淡;21－28d康复组未瘫痪侧脊髓前角较瘫痪侧GAP－43表达的多,而制动组不明显,结论：脑梗塞后康复训练可促进行为恢复及脊髓前角GAP－43表达的增加。     

氦氖激光照射对大鼠神经损伤后脊髓内生长相关蛋白表 …

目的　研究 10mW氦氖 (He Ne)激光照射对大鼠神经损伤后脊髓生长相关蛋白 (growthassociatedprotein ,GAP 43 )表达的影响。 方法　将 96只SD大鼠制成坐骨神经损伤模型 ,用免疫组化方法观察脊髓内GAP 43表达的变化。结果　 1周内激光照射组和对照组无明显差异。 2、4周时照射组脊髓内GAP 43表达明显高于对照组。 8周时激光照射组脊髓内GAP 43表达下降。结论　激光照射可引起损伤神经GAP 43表达的变化 ,有促进完成神经再生的作用。     

大鼠延髓呼吸性神经元向脊髓膈运动神经元投射的实验观察

目的观察大鼠延髓呼吸性神经元向脊髓膈运动神经元的直接投射。方法 2 5只Wistar大鼠分为 3组 :脊髓定位组(5只 )、延髓投射组 (15只 )和对照组 (5只 )。运用辣根过氧化物酶 (HRP)逆追踪法 ,于脊髓定位组膈神经干注入HRP ,确定膈运动神经元在脊髓中的位置 ,然后延髓投射组于逆行性标记细胞位置 ,对照组于脊髓后角分别注入HRP ,观察延髓呼吸性神经元的标记情况。结果在脊髓定位组的注射同侧观察到 ,C3 —C5节段的前角中间部出现逆行性标记细胞 ,为典型的前角运动神经元。在延髓投射组观察到 ,逆行性标识神经元出现在延髓疑后核和面后核的腹内侧部。对照组在上述位置未见标识神经元。结论大鼠膈运动神经元位于C3 -C5节段 ,其投射神经元主要分布在以延髓疑后核和面后核区为主轴的一个长的细胞柱上     

镇痛药的临床应用

一、疼痛的解剖学和神经药理学机制 疼痛的神经传导通路如图1。机体全身皮肤和一些深部组织中广泛存在着痛觉感受器,它们是一些纤细的传入神经纤维的感受伤害的游离神经末梢。机体损伤时,刺激这些神经末梢产生信号经感觉神经传到脊髓后角或三叉神经脊束核,引起后角或相应神经元兴奋。冲动沿脊髓腹外侧索上传,抵达丘脑的外侧和内侧核群。内侧核群的束旁核和中央外侧核被认为是感受疼痛的较高级中枢。由此可通过多突触的联系将疼痛信号传到大脑皮层。某些部位接受的信号,特别是网状结构和延髓,可下行经由多突触     

医学出版物中科技名词术语的规范表达（21）

(每组词在破折号前为宜用词,破折号后为不宜用词,注释从略。)缰核脚间束———后屈束后连合———上丘脑连合背侧丘脑———丘脑丘脑间粘合———中间块外侧核群———背侧核群外侧背核———背侧后核腹中间核———腹外侧核底丘脑———腹侧丘脑医学出版物中科技名词术语的规范表达(21)     

坐骨神经损伤与修复过程中相应脊髓神经元变化的形态学观察

目的探讨坐骨神经损伤与再生修复过程中相应脊髓前角运动神经元的形态学变化和嗅被膜细胞(OECs)对神经元的保护作用。方法采用硅胶管套接切断的大鼠坐骨神经实验模型,将30只大鼠随机分为两组,治疗组硅胶管内注射OECs悬液,对照组注射生理盐水(SAL),应用尼氏法对术后7d、14d、30dSAL组与OECs组脊髓前角运动神经元进行形态学观察,比较两组同类神经元的存活率。结果OECs组治疗侧脊髓前角外侧核大、中型运动神经元的形态结构和存活率与对照组有明显差别。术后7d,OECs组治疗侧神经元数目较SAL组伤侧丢失减少,存活率上升。术后14d和30d,OECs组治疗侧神经元数目较SAL组伤侧明显增加,存活率明显升高,大多数神经元轮廓清楚,尼氏体清晰。结论OECs能减少坐骨神经损伤后相应脊髓前角运动神经元的退行性变。     

腹侧基底丘脑GABA能传递的降低参与慢性炎症痛的发病机制

<正>腹侧基底丘脑(ventrobasal thalamus,VB)包括腹外侧核和腹后中间核,是伤害性信息传递到大脑皮层的重要中继站。已有研究表明,VB核团接受丘脑网状核(thalamic reticular nucleus,TRN)GABA能投射。TRN的GABA能抑制神经元主要通过作用于VB核团中的GABAA受体起调控作用。到目前为止,VB核团GABA能传递是否参与慢性炎症痛的发病机制,尚不清楚。本研究以完全弗氏佐剂(complete Freund's     

坐骨神经损伤后相应脊髓前角运动神经元的形态学变化

目的探讨坐骨神经损伤与修复过程中相应脊髓前角外侧核运动神经元的形态学变化,并对神经元尼氏染色法的应用价值进行评估。方法采用硅胶管套接切断的大鼠坐骨神经模型,应用焦油紫染色、甲苯胺蓝染色和硫堇染色等3种尼氏法对伤后7、14、30d脊髓前角运动神经元进行形态学观察。结果应用3种染色方法均观察到坐骨神经伤侧脊髓前角外侧核大、中型运动神经元的形态结构和存活率与对照侧有明显差别。与对照侧比较,伤后7d伤侧脊髓神经元数目减少,存活率降低;伤后14d和伤后30d,尤其是伤后30d,伤侧脊髓神经元数目减少更显著,存活率下降更明显,有些神经元轮廓不清且尼氏体模糊。结论随着大鼠坐骨神经损伤时间的延长,其相应脊髓前角运动神经元的损伤程度逐渐增加,尤其是伤后30d退变非常明显。焦油紫染色方法是显示神经元尼氏体及反映神经元生活状态的简捷有效的方法。     

The effect of microgene pSVPoMcat to modify Schwann cell on GAP -43 expression after spinal cord injury in adult rats

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微基因修饰雪旺氏细胞移植对大鼠脊髓损伤后GAP－43表达的影响

Objective To study the effect of microgene pSVPoMcat implanted to modify schwann cell on growth associated protein－43(GAP－43) expression after spinal cord injury in adult rats.Method Hemisected of the T8 segment of the spinal cord was performed for all the experiment rats.The rats were randomly divided into three groups as follows:Group A with microgene pSVPoMcat implanted to genetically modify SC;Group B with SC implanted ;Group C with hemisection of the spinal cord only.The changes of expression of GAP－43 in spinal cord were observed by immunochemistry with antibodies against GAP－43 .Simultaneous,the combined behavioral scores(CBS)was measured.Result There were not any different(P >0.05)among the three groups in first week and 12 week.There were significant diffeence(P<0.05)among three groups in 2nd,8th,and more dxpression of GAP－43 at the 2nd week in group A.The neurofunctional recovery was best in group A.Conclusion The microgene pSVPoMcat implanted to modify schwann cell can promote the expression of GAP－43 in spinal cord and functional recovery in adults rats after SCI.     

Inflammation of the hind limb as a model of unilateral, localized pain: influence on multiple opioid systems in the spinal cord of the rat

Inoculation of the right hind paw with Mycobacterium butyricum rapidly led to swelling and inflammation. The afflicted limb showed an enhanced sensitivity to noxious pressure (hyperalgesia) and a reduced sensitivity to noxious heat 24 h following treatment. Both naloxone and MR 2266 (which has greater activity at kappa-opioid receptors) further increased the sensitivity to pressure (that is, potentiated the hyperalgesia) but did not affect the response to heat. They did not affect the response of the uninflamed paw. At 1 week, only MR 2266 was effective. At both 24 h and 1 week, the inflamed paw showed pronounced supersensitivity to the antinociceptive action of morphine against noxious pressure. At both 24 h and (to a greater extent) 1 week, a rise in levels of immunoreactive (ir)-dynorphin (DYN) was seen in the ipsilateral dorsal horn of the lumbar spinal cord. There was no alteration in the contralateral dorsal horn or in either ventral horn. Furthermore, levels of ir-met-enkephalin (ME) and ir-leu-enkephalin (LE) were unaffected. There was no difference in the density of mu-, delta- or kappa-binding sites in any part of the lumbar cord, at either 24 h or 1 week, between ipsilateral and contralateral tissue. By 3 and 5 weeks postinoculation, the symptoms had spread to the contralateral hind limb and ir-DYN was elevated in the contralateral dorsal horn and the ipsilateral ventral horn. At 5 weeks, levels of ir-ME and ir-LE also were increased in the ipsilateral and contralateral dorsal horns, but not in the contralateral ventral horn. Furthermore, levels of ir-DYN were increased in the cervico-thoracic spinal cord, and rats displayed adrenal hypertrophy and a rise in plasma levels of ir-beta-endorphin (beta-EP). These data indicate: (1) Peripheral inflammation localized to a single limb selectively modifies levels of ir-DYN in ipsilateral dorsal horn. The effect is specific to DYN as compared to ME and LE. The density of mu-, delta-, or kappa-receptors in the lumbar spinal cord is unmodified. (2) The altered response to opioid agonists and antagonists shown by rats with an inflamed limb may be selective to the injured tissue. (3) Alterations in opioid systems associated with unilateral hind limb inflammation may not be exclusively chronic in nature: they appear very rapidly (within 24 h) of the induction of pain. With time, the contralateral limb becomes affected and, eventually, the effects resemble those seen with generalized polyarthritis.     

Changes in brain functional activation during resting and locomotor states after unilateral nigrostriatal damage in rats

To evaluate functional neuronal compensation after partial damage to the nigrostriatal system, we lesioned rats unilaterally in the striatum with 6-hydroxydopamine. Five weeks later, cerebral perfusion was mapped at rest or during treadmill walking using [(14)C]-iodoantipyrine. Regional CBF-related tissue radioactivity (CBF-TR) was quantified by autoradiography and analyzed by statistical parametric mapping and region-of- interest analysis. Lesions were confirmed by tyrosine hydroxylase immunohistochemistry and changes in rotational locomotor activity. Functional compensations were bilateral and differed at rest and during treadmill walking. Consistent with the classic view of striatopallidal connections, CBF-TR of lesioned compared to sham-lesioned rats increased in the ipsilateral subthalamic nucleus (STN) and internal globus pallidus, and decreased in the striatum and external globus pallidus. Contrary to the classic view, CBF-TR increased in the ipsilateral ventral lateral, ventral anterior thalamus and motor cortex, as well as in the central medial thalamus, midline cerebellum, and contralateral STN. During walking, perfusion decreased in lesioned compared to sham-lesioned rats across the ipsilateral striato-pallidal-thalamic-cortical motor circuit. Compensatory increases were seen bilaterally in the ventromedial thalamus and red nucleus, in the contralateral STN, anterior substantia nigra, subiculum, motor cortex, and in midline cerebellum. Enhanced recruitment of associative sensory areas was noted cortically and subcortically. Future models of compensatory changes after nigrostriatal damage need to address the effects of increased neural activity by residual dopaminergic neurons, interhemispheric interactions and differences between resting and locomotor states. Identification of sites at which functional compensation occurs may define useful future targets for neurorehabilitative or neurorestorative interventions in Parkinson's disease.     

运动训练对大鼠损伤远端脊髓超微结构及脑源性神经营养因子表达的影响

目的:明确运动训练对大鼠脊髓损伤(SCI)后远端脊髓超微结构及脑源性神经营养因子(BDNF)表达的影响。方法:成年雌性SD大鼠18只,采用改良Allen撞击法制作T9不完全性SCI模型。术后随机分为损伤后1周组、对照组(未行训练)及训练组(术后1周开始训练,共4周)。分别在损伤前、损伤后第1、2、3、4及5周时采用BBB评分评定运动功能,训练结束后取腰膨大段脊髓进行电镜观察超微结构,免疫组化检测BDNF蛋白表达情况。结果:①BBB评分:对照组与训练组BBB评分均较损伤后1周、2周明显提高,但训练组较对照组增加更为显著(P<0.05)。②超微结构:损伤后1周组,髓鞘排列规律整齐、轴索较均匀一致、核仁清晰;对照组髓鞘松散、轴索与髓鞘间出现空隙、轴突变性及空泡;训练组髓鞘完整、较薄、轴索均匀、髓鞘下及神经纤维周围基质中少见空泡。③BDNF免疫组化:BDNF免疫反应阳性产物多分布于脊髓前角,中央管周围也有出现,背角少见;训练组BDNF阳性染色颗粒增多,平均光密度值较损伤后1周组及对照组均显著增加(P<0.05)。结论:运动训练能减轻损伤远端脊髓继发性损害,并促进BDNF蛋白的表达。     

高压氧前处理脊髓损伤大鼠前角运动神经元的凋亡

背景：脊髓损伤后难以修复,损伤后保护残存的神经元是促进神经再生的关键。目的：验证高压氧预处理可以通过抑制早期的细胞凋亡来保护脊髓前角运动神经元。方法：随机将26只雄性Wistar大鼠等分成模型组和实验组。实验组在给予高压氧5d后与模型组同时制作脊髓T9~10全横断模型。结果与结论：尼氏染色显示脊髓T9~T10全横断后8h及1d,脊髓前角的浓染的细胞多见,与模型组相比,实验组脊髓前角浓染的细胞较少。TUNEL染色也显示脊髓T9~T10全横断后脊髓损伤后8h~1d,2组大鼠脊髓前角内均可见大量的凋亡神经元,3d时凋亡神经元数量减少。相比于模型组,高压氧预处理8h,1d后大鼠脊髓前角凋亡神经元较少（P〈0.05,P〈0.01）。说明高压氧预处理能对脊髓损伤后前角运动神经元起保护作用。     

高压氧前处理脊髓损伤大鼠前角运动神经元的凋亡

背景:脊髓损伤后难以修复,损伤后保护残存的神经元是促进神经再生的关键。目的:验证高压氧预处理可以通过抑制早期的细胞凋亡来保护脊髓前角运动神经元。方法:随机将26只雄性Wistar大鼠等分成模型组和实验组。实验组在给予高压氧5d后与模型组同时制作脊髓T9~10全横断模型。结果与结论:尼氏染色显示脊髓T9~T10全横断后8h及1d,脊髓前角的浓染的细胞多见,与模型组相比,实验组脊髓前角浓染的细胞较少。TUNEL染色也显示脊髓T9~T10全横断后脊髓损伤后8h~1d,2组大鼠脊髓前角内均可见大量的凋亡神经元,3d时凋亡神经元数量减少。相比于模型组,高压氧预处理8h,1d后大鼠脊髓前角凋亡神经元较少(P<0.05,P<0.01)。说明高压氧预处理能对脊髓损伤后前角运动神经元起保护作用。     

电针对神经病理性疼痛大鼠痛觉过敏及脊髓背角钾-氯离子协同转运体2表达的影响

目的:观察患侧电针和健侧电针足三里穴、阳陵泉穴对神经病理性疼痛大鼠行为学表现以及脊髓背角钾-氯离子协同转运体2(KCC2)表达的影响,探讨患侧选穴和健侧选穴两种针刺方案的镇痛效应,以及KCC2在电针镇痛效应中的作用。方法:将40只雄性SD大鼠随机分为4组:假模组、模型组、患侧电针组、健侧电针组,每组10只。建立大鼠坐骨神经慢性压迫性损伤(CCI)模型,治疗组于术后1周开始电针治疗,每天1次,连续7天。各组于术前(0天)及术后3、5、7、10、12、14天分别测量大鼠患侧足机械足反射阈值(MWT)和热缩足反射潜伏期(TWL)。术后14天处死大鼠,取脊髓组织行HE染色观察组织病理学改变,并采用免疫组化方法检测脊髓背角KCC2蛋白的表达。结果:与术前比较,CCI各组大鼠痛阈明显降低,出现痛觉过敏(P0.001),电针治疗后大鼠MWT和TWL均有不同程度的持续升高,且患侧与健侧电针相比无明显差异。HE染色结果提示,患侧电针组与健侧电针组脊髓背角组织及神经元病变程度较模型组减轻。术后14天患侧与健侧电针组较模型组脊髓背角患侧KCC2表达显著增加(P0.05),并且患侧电针组与健侧电针组无明显差异。结论:患侧电针和健侧电针能产生类似的镇痛效果,均可减轻外周神经损伤后引起的痛觉过敏。患侧电针与健侧电针治疗均可抑制KCC2蛋白的表达下调,电针的镇痛作用可能是通过增加脊髓背角中KCC2的表达实现的。