褪黑素对阿茨海默病大鼠海马突触素表达的影响

目的 研究褪黑素(melatonin,MT)对阿茨海默病(Alzheimer's disease , AD)大鼠的海马突触素表达的影响.方法 大鼠随机分为4组,分别为AD组、AD-MT大剂量干预组、AD-MT小剂量干预组和假AD组.应用β-淀粉样蛋白(Aβ)注入大鼠海马CA1区,建立大鼠AD模型,AD-MT干预组随之以MT灌胃,1次/d,直至试验结束.应用电迷宫检测大鼠学习记忆情况,用免疫组化方法检测大鼠海马CA1区突触素的表达情况.结果 MT可以明显改善AD大鼠的学习记忆能力,提高大鼠海马CA1区突触素的阳性表达.结论 MT对AD大鼠有显著脑保护作用.     

大鼠脑内基质金属蛋白酶-9表达及其在海马依赖的学习记忆中的作用

目的:探讨Y迷宫训练后大鼠脑内基质金属蛋白酶-9(MMP-9)表达及其在海马依赖的学习记忆中的作用.方法:3月龄雄性SD大鼠,随机分成对照组(n=12)和Y迷宫训练组(n=60),后者又根据训练天数和处死时间分成5个亚组.计算大鼠在Y迷宫训练中的连续正确反应次数,观察其学习能力;用Western blot检测各组大鼠不同脑区MMP-9前体蛋白(proMMP-9)和活性形式(actMMP-9)的蛋白表达,用免疫组化学和RT-PCR分别检测海马区MMP-9蛋白和mRNA的表达.探讨MMP-9表达与其学习能力的相关性.结果:①Y迷宫训练早期,大鼠海乌区出现actMMP-9蛋白水平一过性增加,同时其MMP-9 mRNA表达也相应升高;而额叶区未出现类似变化.②Y迷宫第1天训练后4h大鼠海马区actMMP-9表达水平与其第1天训练成绩(平均连续正确反应次数)呈正相关(P<0.05).结论:actMMP-9可能参与了大鼠Y迷宫的学习过程.     

17β-雌二醇对血管性痴呆大鼠海马CA1区神经突触可塑性的影响

目的探讨突触可塑性在17p雌二醇改善血管性痴呆（VD）大鼠认知功能障碍中所起的作用。方法选用〉16月龄雄性Wistar大鼠,应用Y迷宫进行空间定向学习和记忆训练,将达到标准者随机分为3组：（1）假手术（Sham）组;（2）VD组;（3）VD＋雌二醇腹部皮下注射（E）组。应用免疫组织化学染色及RT—PCR的方法,检测大鼠海马CA1区微管相关蛋白2（MAP-2）和突触素（SYN）蛋白含量和mRNA表达水平的改变。结果术后60d,E组和VD组MAP-2和SYN表达均有下降,但VD组下降更为明显。结论17β-雌二醇相对增加VD大鼠海马CA1区MAP-2、SYN蛋白含量和mRNA的表达。提示相对增加与突触可塑性相关的MAP-2、SYN蛋白含量和mRNA的表达,可能是雌二醇改善VD认知功能障碍的机制之一。     

血管性痴呆大鼠海马突触素、发动蛋白Ⅰ的mRNA及蛋白表达变化

目的探讨血管性痴呆(VaD)大鼠海马突触素、发动蛋白Ⅰ的mRNA及蛋白表达变化。方法利用改良四血管法制备血管性痴呆大鼠模型。通过Morris水迷宫观察大鼠空间探索及学习记忆情况,采用Real-time及Western-blot法分别检测大鼠海马突触素、发动蛋白Ⅰ的mRNA与蛋白水平,并与假手术组进行比较。结果 VaD组大鼠各时间点平均逃避潜伏期及第1次穿越平台所用时间均显著长于假手术组(均P0.01),平台穿越次数明显减少(P0.05)。VaD组海马突触素及发动蛋白Ⅰ蛋白表达及mRNA表达显著低于假手术组(P0.05~0.01)。结论脑缺血引起大鼠海马组织突触素、发动蛋白Ⅰ表达降低,可能与VaD发病中学习记忆能力减退有关。     

学习记忆训练对全脑缺血大鼠认知能力的影响

目的探讨学习记忆训练对全脑缺血大鼠空间学习记忆能力的影响及检测脑源性神经营养因子的变化。方法选用健康雄性SD大鼠90只随机分为假手术组、对照组和训练组,采用改良Pulsinelli’s 4血管闭塞法(4-VO)制作全脑缺血大鼠模型,术后1周以Y型电迷宫训练大鼠,分别在训练7d、14d、21d后应用Y型电迷宫检测比较3组大鼠的空间学习记忆能力的差异;HE染色观察CA1区神经元变化;免疫组化检测脑源性神经营养因子的表达。结果训练21d后,对照组与假手术组和训练组比较,Y型电迷宫全天总反应时间和潜伏期明显延长(P<0.05),错误反应次数明显增多(P<0.05)。对照组CA1区脑源性神经营养因子的光密度值明显低于训练组(P<0.05)。结论学习记忆训练可以改善全脑缺血大鼠的空间学习记忆能力,提示应用学习记忆训练方法可以改善全脑缺血损伤后引起的学习记忆障碍。     

行为学训练对低剂量X线照射后SD大鼠认知能力的改善作用研究

目的 探讨行为学训练对低剂量X线照射后幼年SD大鼠学习记忆的影响及其相关机制. 方法 出生后35d的SD大鼠按抽签法随机分为训练组、照射组及对照组,每组各16只.照射组、训练组每天均接受1次低剂量[以临床中婴幼儿(0～6岁)所采用剂量为基准]X线照射,共7d.对照组接受假照射.通过Morris水迷宫训练其学习记忆能力,7.0T MR检测3组大鼠海马区N-乙酰-天门冬氨酸/肌酸(NAA/Cr)比值.荧光免疫组化法和Western blotting检测各组大鼠海马区细胞色素C氧化酶亚基Ⅳ(COXⅣ)蛋白表达的变化.HE染色观察海马CA1区神经元形态,透射电镜观察神经元线粒体形态. 结果 (1)照射组NAA/Cr值(1.611±0.013)较对照组(1.873±0.032)明显降低,训练组NAA/Cr值(1.870±0.018)较照射组明显升高,差异均有统计学意义(P＜0.05).(2)定位航行实验中照射组大鼠第1～4天逃避潜伏期均长于对照组大鼠,差异有统计学意义(P＜0.05);训练组大鼠第1～4天逃避潜伏期与对照组大鼠无明显区别,差异无统计学意义(P＞0.05).空间探索实验中,照射组大鼠穿越原站台次数、原站台象限停留时间均明显少于对照组,差异有统计学意义(P＜0.05);训练组大鼠穿越原站台次数、原站台象限停留时间与对照组大鼠无明显区别,差异无统计学意义(P＞0.05).(3)荧光免疫组化结果显示照射组大鼠海马CA1区COXⅣ蛋白表达减少,训练组COXⅣ表达增加.Western blotting结果显示照射组大鼠海马CA1区COXⅣ蛋白表达(0.298±0.049)较对照组(0.998±0.056)明显减少,差异有统计学意义(P＜0.05);训练组COXⅣ表达(0.987±0.053)接近训练组,差异无统计学意义(P＞0.05).(4)照射组大鼠可见核固缩及较多受损的线粒体,训练组大鼠仅见少量受损线粒体. 结论 行为学训练可能通过增加COXⅣ蛋白表达,改善线粒体形态及功能来恢复低剂量X线照射后幼年SD大鼠受损的学习记忆能力.     

吗啡戒断性焦虑大鼠海马突触界面结构及突触素表达变化

目的 探讨吗啡依赖戒断焦虑行为与海马CA1、CA3区突触界面结构和突触素表达变化之间的相关性.方法 剂量递增法建立大鼠吗啡依赖模型,高架十字迷宫检测焦虑行为,透射电镜技术结合图像分析系统、免疫组织化学比较对照组、模型组和治疗组(各6只)大鼠海马CA1、CA3区突触界面结构和突触素(P38)的表达.结果 (1)行为学:模型组开放臂的次数和时间均少于对照组和治疗组[最小有意义差异t检验(下同),P＜0.01或P＜0.05).(2)突触界面结构:模型组CA1区突触后致密物厚度[(10.7±0.9)nm]、突触活性区长度[(45±4)am]、突触间隙宽度[(3.80±0.30)nm]和突触界面曲率(1.37±0.12)均高于对照组和治疗组(P＜0.01或P＜0.05);模型组CA3区突触后致密物厚度[(12.7±1.1)nm]、突触活性区长度[(53±8)nm]、突触间隙宽度[(3.81 ±0.59)nm]、突触界面曲率(1.39±0.30)亦均高于对照组和治疗组(P＜0.01或P＜0.05).(3)突触素表达:模型组CA1、CA3区突触素吸光度(A)值分别为(0.42±0.06)和(0.43±0.05),显著高于对照组(0.2±0.02,0.25±0.03)和治疗组(0.27±0.04,0.26±0.03).结论吗啡戒断焦虑行为与海马CA1、CA3区突触形态结构可塑性及突触素表达水平有一定的相关性.     

慢性脑缺血老龄大鼠海马中突触素的表达特征

目的 研究老龄大鼠慢性脑缺血后大脑海马中突触素表达特征.方法 应用免疫组化染色技术检测大鼠脑海马中CA1区、CA3区和齿状回中突触素的表达.结果 缺血组海马CA1区、CA3区和齿状回三处突触素灰度值均低于对照组,差异有统计学意义(P<0.05.结论 老龄大鼠海马结构内CA1区、CA3区及齿状回内突触素和NR2B的表达明显减少.     

三磷酸胞苷二钠对脑缺血大鼠海马CA3区突触体素表达的影响

目的　研究局灶性脑缺血后海马 CA3 区突触体素的动态表达及其三磷酸胞苷二钠对其干预的影响。方法　选取 SD大鼠 60只 ,随机分为脑缺血后自然恢复组、药物干预组和假手术对照组。采用线栓法建立大脑中动脉脑缺血大鼠模型 ,应用免疫组化技术观察海马 CA3 区突触体素的表达。结果　脑缺血后自然恢复组大鼠突触体素的表达较对照组明显降低 (P<0 .0 1) ;但 7～ 2 1d突触体素的表达逐渐上调 (P<0 .0 1)。应用三磷酸胞苷二钠干预后 ,突触体素表达与自然恢复组相比明显升高。结论　脑缺血损伤后海马 CA3 区突触体素表达减少 ,但机体自身存在着神经元的修复和再生 ;三磷酸胞苷二钠可上调突触体素的表达 ,具有促进缺血神经元的修复、再生及突触重塑作用。     

丁基苯酞对慢性脑缺血老龄大鼠海马中NMDA受体亚单位NR2B及突触素表达的影响

目的 观察丁基苯酞对慢性脑缺血老龄大鼠海马中N-甲基-D-天门冬氨酸受体2B亚单位(NR2B)及突触素表达的影响.方法 采用免疫组化方法观察丁基苯酞对慢性脑缺血老龄大鼠海马中NR2B及突触素表达的影响.结果 B组与A组比较,海马CA1区、CA3区及齿状回NR2B及突触素的表达明显减少(P＜0.05),C、D组大鼠海马各区NR2B及突触素的表达与单纯缺血组比较均不同程度增加(P＜0.05);D组与C组比较,NR2B及突触素的表达增加更明显(P＜0.05).结论 慢性缺血3个月后,大鼠海马CA1区、CA3区及齿状回中NR2B 及突触素的表达明显减少,而丁基苯酞能改善这种缺血改变,增加NR2B 及突触素的表达.     

创伤性癫痫大鼠前脑海马CA3区突触蛋白表达与突触重建的相关性

摘要 目的：动态观察突触后密度蛋白-95(PSD-95)和突触囊泡蛋白(SYN)在外伤性癫痫(PTE)大鼠前脑的表达,探讨有关发病机制。方法：立体定向注射1000 nmol FeCl2：于大鼠右侧运动皮层致痫,在不同时间点行为学视频、脑电图监测,用免疫组织化学法检测24h、7d、14d、21d、30d大鼠前脑内PSD-95及SYN的表达。结果;所有大鼠在注射FeC12后不久记录到癫痫样放电,7d达高峰;致痫后24h即可见前脑神经元PSD-95表达下降,7d达最低值,14d后回升;SYN表达在24h明显下降,7d后逐渐回升。结论：FeC12皮层注射可以制成PTE动物模型。与PSD-95 及SYN表达相关的神经元及胶质细胞的动态变化在PTE的发病机制中起重要作用。PSD-95和SYN表达减少可能为FeCl2致痫的共同途径。     

Hippocampal microtubule-associated protein-2 alterations with contextual memory

Using immunohistochemistry and immunoblots, we show that alterations in hippocampal microtubule-associated protein-2 appear to be highly correlated with contextual memory as measured by significantly heightened fear responses. Compared to naive controls, rats trained in a novel context showed significantly increased immunostaining for the high molecular weight microtubule-associated protein-2a/b. This increase was observed 2 weeks after training and it was selective for hippocampal CA1 and CA2 pyramidal cells. Pre-exposure to the training context one month before training altered the hippocampal microtubule-associated protein-2 response; in these animals only the dentate gyrus showed significantly increased microtubule-associated protein-2a/b. Training-related increases in immunohistochemical staining for microtubule-associated protein-2 suggested that there was an increase in overall intact protein, an increase in immunoreactive breakdown products, or changes in protein compartmentalization. Immunoblots of hippocampal homogenates reacted with monoclonal antibodies to microtubule-associated protein-2a/b showed an increased presence of breakdown products in trained animals compared to untrained controls. Additional immunoblot studies demonstrated statistically significant decreases in the levels and/or phosphorylation state of the low molecular weight microtubule-associated protein-2c in the hippocampus of trained animals as compared to that of controls. These alterations in microtubule-associated protein-2 may reflect dendritic remodeling related to contextual memory storage.     

Exercise preconditioning exhibits neuroprotective effects on hippocampal CA1 neuronal damage after cerebral ischemia

Recent evidence has suggested the neuroprotective effects of physical exercise on cerebral ischemic injury. However, the role of physical exercise in cerebral ischemia-induced hippocampal damage remains controversial. The aim of the present study was to evaluate the effects of pre-ischemia treadmill training on hippocampal CA1 neuronal damage after cerebral ischemia. Male adult rats were randomly divided into control, ischemia and exercise + ischemia groups. In the exercise + ischemia group, rats were subjected to running on a treadmill in a designated time schedule(5 days per week for 4 weeks). Then rats underwent cerebral ischemia induction th rough occlusion of common carotids followed by reperfusion. At 4 days after cerebral ischemia, rat learning and memory abilities were evaluated using passive avoidance memory test and rat hippocampal neuronal damage was detected using Nissl and TUNEL staining. Pre-ischemic exercise significantly reduced the number of TUNEL-positive cells and necrotic cell death in the hippocampal CA1 region as compared to the ischemia group. Moreover, pre-ischemic exercise significantly prevented ischemia-induced memory dysfunction. Pre-ischemic exercise mighct prevent memory deficits after cerebral ischemia through rescuing hippocampal CA1 neurons from ischemia-induced degeneration.     

针刺预处理对短暂性脑缺血再灌注损伤海马神经元的保护

The present study established a model of brain ischemia in aged rats using four-vessel occlusion.We observed hippocampal CA1 neuronal apoptosis and apoptosis-mediated protease caspase-3 expression following preconditioning of electroacupuncture at Baihui(GV 20).Our results showed that the number of hippocampal CA1 normal neurons was decreased,and degenerated neurons were increased 12 hours to 3 days following cerebral ischemia/reperfusion.The number of hippocampal CA1 apoptotic neurons and caspase-3-positive neurons in rats with cerebral ischemia/reperfusion injury was significantly decreased following acupuncture preconditioning.Acupuncture preconditioning protects aged rats against ischemia/reperfusion injury by regulating caspase-3 protein expression.     

Selective vulnerability of hippocampal CA3 neurons to hypoxia after mild concussion in the rat

Immunohistochemical staining for microtubule-associated protein 2 (MAP2) and synaptophysin was used to investigate the effect of hypoxia on hippocampal neurons after mild concussion in the rat. Male Sprague-Dawley rats were divided into four groups: Group 1 (n = 3) was subjected to a mild impact-acceleration closed head injury group 2 (n = 3) was subjected to 30 min of moderate hypoxia, group 3 (n = 5) was subjected to head trauma followed by 30 min of moderate hypoxiaand group 4 (n = 3) comprised sham-operated controls. All rats were fixed by transcardial perfusion 24 h after insult. No damage was observed in CA1 or CA2 neurons in any of the rats. However, rats in group 3 showed selective damage of hippocampal CA3 neurons manifested by a pycnosis and a marked decrease in MAP2 immunoreactivity. Presynaptic terminals visualized by synaptophysin immunostaining showed no differences among groups. The loss of immunoreactivity for the post-synaptic somal and dendritic protein marker MAP2 from the CA3 subfield 24 h after combined insults indicates an increased vulnerability of pyramidal cells in this brain area. [Neurol Res 1995; 17: 455-460]     

Effects of exogenous ganglioside-1 on learning and memory in a neonatal rat model of hypoxia-ischemia brain injury★

BACKGROUND: Exogenous ganglioside-1 (GM1) can cross the blood-brain barrier and play a protective role against hypoxia-ischemia-induced brain damage. OBJECTIVE: To examine the possible mechanisms of exogenous GM1 protection in hypoxia-ischemia-induced brain damage in a neonatal rat model by measuring changes in brain mass, pathological morphology, growth-associated protein-43 expression, and neurobehavioral manifestations. DESIGN, TIME AND SETTING: A randomized block-design study was performed at the Immunohistochemistry Laboratory of the Pediatric Research Institute, Children’s Hospital of Chongqing Medical University from August 2005 to August 2006. MATERIALS: A total of 36 neonatal, 7-day-old, Sprague Dawley rats were used in this experiment. The hypoxia-ischemia-induced brain damage model was established by permanently occluding the right carotid artery, followed by oxygen inhalation at a low concentration (8% O2, 92% N2) for 2 hours. METHODS: All rats were randomly divided into the following groups: GM1, model, and sham operation, with 12 rats each group. Rats in the GM1 and model groups received hypoxic/ischemic-induced brain damage. Rats in the GM1 group received injections of GM1 (i.p., 20 mg/kg) at 0, 24, 48, 72, 96, 120, and 144 hours following models established, and rats in the model group were administered (i.p.) the same amount of saline. The right carotid artery was separated, but not ligated, in the sham operation group rats. MAIN OUTCOME MEASURES: At 1 week after surgery, expression of growth-associated protein-43, a marker of neural development and plasticity, was detected in the hippocampal CA3 region by immunohistochemistry. Brain mass was measured, and the pathological morphology was observed. At 4 weeks after surgery, behavioral changes in the remaining rats were tested by Morris water maze, and growth-associated protein-43 expression was measured. RESULTS: (1) In the GM1 and sham operation groups, growth-associated protein-43 expression was greater in the hippocampal CA3 region compared to the model group 1 week after surgery (P < 0.05). In all three groups, brain weight of the right hemisphere was significantly less than the left hemisphere, in particular in the model group (P < 0.05). In the GM1 group, the weight difference between two hemispheres, as well as the extent of damage in the right hemisphere, was less than the model group (P < 0.01). In the sham operation group, brain tissue consisted of integrated structures and ordered cells. In the model group, the cerebral cortex layers of the right hemisphere were not defined, neurons were damaged, and neurons were disarranged in the hippocampal area. In the GM1 group, neurons were dense in the right cerebral cortex and hippocampal area, with no significant change in glial proliferation. (2) The average time of escape latency in the GM1 group was shortened 4 weeks after surgery, and significantly less than the model group (P < 0.05). In addition, the frequency platform passing in the GM1 group was significantly greater than the model group (P < 0.01). CONCLUSION: Exogenous GM1 may reduce brain injury and improve learning and memory in hypoxia-ischemia-induced brain damage rats. This protection may be associated with increased growth-associated protein-43 expression, which is involved in neuronal remodeling processes. Key Words: ganglioside; growth-associated protein-43; hypoxia-ischemia brain damage; Morris water maze     

Intercellular adhesion molecule-1 expression in the hippocampal CA1 region of hyperlipidemic rats with chronic cerebral ischemia

Chronic cerebral ischemia is a pathological process in many cerebrovascular diseases and it is induced by long-term hyperlipidemia,hypertension and diabetes mellitus.After being fed a high-fat diet for 4 weeks,rats were subjected to permanent occlusion of bilateral common carotid arteries to establish rat models of chronic cerebral ischemia with hyperlipidemia.Intercellular adhesion molecule-1 expression in rat hippocampal CA1 region was determined to better understand the mechanism underlying the effects of hyperlipidemia on chronic cerebral ischemia.Water maze test results showed that the cognitive function of rats with hyperlipidemia or chronic cerebral ischemia,particularly in rats with hyperlipidemia combined with chronic cerebral ischemia,gradually decreased between 1 and 4 months after occlusion of the bilateral common carotid arteries.This correlated with pathological changes in the hippocampal CA1 region as detected by hematoxylin-eosin staining.Immunohistochemical staining showed that intercellular adhesion molecule-1 expression in the hippocampal CA1 region was noticeably increased in rats with hyperlipidemia or chronic cerebral ischemia,in particular in rats with hyperlipidemia combined with chronic cerebral ischemia.These findings suggest that hyperlipidemia aggravates chronic cerebral ischemia-induced neurological damage and cognitive impairment in the rat hippocampal CA1 region,which may be mediated,at least in part,by up-regulated expression of intercellular adhesion molecule-1.     

Hippocampal expression of synaptic structural proteins and phosphorylated cAMP response element-binding protein in a rat model of vascular dementia induced by chronic cerebral hypoperfusion

The present study established a rat model of vascular dementia induced by chronic cerebral hypoperfusion through permanent ligation of bilateral common carotid arteries.At 60 days after modeling,escape latency and swimming path length during hidden-platform acquisition training in Morris water maze significantly increased in the model group.In addition,the number of accurate crossings over the original platform significantly decreased,hippocampal CA1 synaptophysin and growth-associated protein 43 expression significantly decreased,cAMP response element-binding protein expression remained unchanged,and phosphorylated cAMP response element-binding protein expression significantly decreased.Results suggested that abnormal expression of hippocampal synaptic structural protein and cAMP response element-binding protein phosphorylation played a role in cognitive impairment following chronic cerebral hypoperfusion.     

Altered protein markers related to neural plasticity and motor function following electro-acupuncture treatment in rat model of ischemic-hypoxic brain injury

BACKGROUND: Previous studies have demonstrated that acupuncture treatment could ameliorate impaired motor function, and these positive effects might be due to neural plasticity. OBJECTIVE: Myelin basic protein (MBP), microtubule-associated protein 2 (MAP2), growth-associated protein-43 (GAP-43), and synaptophysin (SYN) were selected as markers of neural remodeling, and expression of these markers was evaluated with regard to altered motor function following brain injury and acupuncture treatment. DESIGN, TIME AND SETTING: A completely randomized experiment was performed at the Central Laboratory of Peking University First Hospital from November 2006 to May 2007. MATERIALS: Twenty-four Sprague Dawley rat pups, aged 7 days, were selected for the present experiment. The left common carotid artery was ligated to establish a rat model of ischemic-hypoxic brain injury.METHODS: All animals were randomly divided into three groups: sham operation, model, and electro-acupuncture treatment, with 8 rats in each group. Rats in the model and electro-acupuncture treatment group underwent establishment of ischemic-hypoxic brain injury. Upon model established, rats underwent hypobaric oxygen intervention for 24 hours. Only the left common carotid artery was exposed in rats of the sham operation group, without model establishment or oxygen intervention. The rats in the electro-acupuncture treatment group were treated with electro-acupuncture. One acupuncture needle electrode was inserted into the subcutaneous layer at the Baihui and Dazhui acupoint. The stimulation condition of the electro-acupuncture simulator was set to an amplitude-modulated wave of 0-100% and alternative frequency of 100 cycles/second, as well as frequency-modulated wave of 2-100 Hz and an alternative frequency of 3 cycles/second. Maximal current through the two dectrodes was limited to 3-5 mA. The stimulation lasted for 30 minutes per day for 2 weeks. Rats in the sham operation and model groups were not treated with electro-acupuncture, but only fixed to the table for the same time period. MAIN OUTCOME MEASURES: After 2 weeks stimulation, expression of MBP, MAP2, GAP-43, and SYN were detected in the brain by immunohistochemistry. Motor function was evaluated in the three groups. RESULTS: In the sham operation group, MBP was abundant in the myelinated nerve fibers. In the electro-acupuncture treatment group, however, the corpus callosum exhibited more MBP staining than the model group. MAP2 expression was increased in the model group, and increased further in the electro-acupuncture treatment group compared with the sham operation group. GAP-43 expression in the cerebral cortex was less in model group than in sham operation, but present in abundance in the electro-acupuncture treatment group. SYN expression in the cerebral cortex was less in the model and electro-acupuncture treatment group compared with the sham operation group. There was no significant difference in SYN expression and distribution between the model and electro-acupuncture treatment groups. Motor function of rats in the electro-aeapuncture treatment group was significantly better than the model group (P < 0.05), although function remained lower than the sham operation group (P < 0.05). CONCLUSION: Two weeks of electro-acupuncture treatment improved motor function in rats, and protein markers related to neural plasticity also changed, which may be a mechanism for improved motor function in rats with ischemic-hypoxic brain injury.