慢性间歇性缺氧对幼年大鼠认知功能的影响及机制研究

目的 观察慢性间歇性缺氧对幼年大鼠认知功能的影响并探讨其发生机制.方法 （20±2）日龄SD雄性大鼠40只,随机分为正常组和慢性间歇性缺氧组.将慢性间歇性缺氧组幼鼠置入自制缺氧舱内每天缺氧8h,连续缺氧2周,建立模型后,利用Morris水迷宫检测认知功能的变化,记录海马CA1区神经元自发放电频率和幅度,利用HE染色和免疫组化法观察海马结构改变和GAP-43的表达情况.结果 与正常组比较,慢性间歇性缺氧组体重较轻（P＜0.05）,在Morris水迷宫测试中逃避潜伏期明显延长（P＜0.05）,穿越平台次数明显减少（P＜0.05）;海马CA1区神经元自发放电频率、波幅减小（P＜0.05）,海马CA1区出现明显的损伤,GAP-43表达增高（P＜0.05）.结论 慢性间歇性缺氧可引起幼年大鼠认知功能损伤,而海马神经元突触可塑性的改变可能是认知功能损伤的机制.     

内侧隔核胆碱能神经元参与SNI神经病理性疼痛大鼠模式分离障碍

目的:研究部分神经损伤(spared nerve injury, SNI)神经病理性疼痛大鼠导致模式分离(pattern separation)障碍的机制。方法:实验分为两部分,第一部分实验大鼠分为两组:假手术(sham SNI)组、SNI组;第二部分实验大鼠分为两组:假损毁、SAP损毁。首先制作SNI神经病理性疼痛模型,之后用八臂迷宫进行模式分离实验来比较sham SNI和SNI实验组大鼠的空间认知水平。此外用SAP (192Ig G-saporin)的方式损毁内侧隔核(medial septum, MS)内的胆碱能神经元,用八臂迷宫来比较损毁组和对照组大鼠的模式分离变化。结果:SNI组大鼠在八臂迷宫中的正确率明显低于sham SNI组,并且SNI导致内侧隔核内的胆碱能神经元数目降低,而损毁MS内胆碱能神经元后大鼠八臂迷宫的正确率明显低于假损毁组。结论:SNI神经病理性疼痛导致模式分离障碍可能与内侧隔核中的胆碱能神经元有关。     

右侧额顶网络在空间注意认知过程中的作用机制

目的:探讨右侧额顶网络(FPN)与视空间注意认知功能的关联性和作用机制.方法:选取志愿受试者60人参加本实验,随机分为顶叶组和额叶组.采用持续短阵快速脉冲(cTBS)经颅磁刺激(rTMS)右侧背外侧前额叶(DLPFC)和后顶叶皮质(DPC)后进行注意网络测试(ANT),所有受试者均按照随机顺序进行真/假刺激.结果:持续短阵快速脉冲经颅磁刺激施加于前额叶和后顶叶,不同提示和刺激类型的平均反应时均无明显改变.右侧后顶叶抑制,警觉和定向功能受损(P＜0.05);右侧额叶抑制,执行功能受损(P＜0.05),而定向功能增强(P＜0.05).结论:在视空间注意过程中,右侧后顶叶是定向功能的关键区,右侧前额叶是执行功能的关键区,并且右侧额顶区之间存在竞争性抑制现象.     

唑尼沙胺对癫痫小鼠学习记忆及海马神经元的影响

目的探讨应用唑尼沙胺对癫痫小鼠空间学习、记忆能力的影响,并观察海马组织形态学的改变。方法60只小鼠随机分为正常对照组和模型组,模型组采用腹腔注射戊四氮(45 mg/kg)复制癫痫动物模型。筛选造模合格小鼠30只随机分为癫痫模型组、唑尼沙胺组,各15只。正常对照组、癫痫模型组每日经口腔灌胃0.9%的氯化钠溶液0.15 ml,唑尼沙胺组经口腔灌胃溶于0.9%氯化钠溶液的唑尼沙胺(75 mg/kg)。观察各组小鼠行为表现,2周后行Morris水迷宫实验5 d,结束后取海马组织切片行HE染色,光学镜下观察海马组织形态学变化。结果与癫痫模型组比较,唑尼沙胺组在定位航行和空间探索时间均有明显提升,差异有统计学意义(P0.05),而与正常组比较差异无统计学意义(P0.05);且唑尼沙胺能够减轻海马神经元细胞损伤。结论唑尼沙胺能够延长惊厥发作潜伏期,缩短发作持续时间,减少自发发作次数,降低致痫小鼠的惊厥发作级别,进而减轻脑组织神经元损伤程度,改善癫痫小鼠的认知功能。     

维生素A缺乏影响胶质源性神经营养因子抑制大鼠缺氧缺血脑损伤后细胞增殖的研究

目的:研究体内维生素A水平缺乏通过RARα通路抑制大鼠缺氧缺血性脑损伤(HIBD)后神经细胞增殖进而影响脑组织功能恢复。方法:将74只SD大鼠随机分为假手术组(CON组)、VA正常(VAN组)及VA缺乏组(VAD组),HIBD建模按经典Rice法。Morris水迷宫评估空间记忆力,EDU细胞增殖检测VAN、VAD组HIBD后细胞增殖,更深入剖析皮质组织RA受体、神经标志物的基因水平。结果:Morris水迷宫实验提示HIBD后恢复晚期VAN组空间记忆力明显强于VAD组(P0.05);EDU结果显示,VAN组新生细胞增殖明显强于VAD组(P0.05);RARα是各RA受体表达的优势受体。VAN组巢蛋白(Nestin)、神经元特异性烯醇化酶(NSE)、胶质纤维酸性蛋(GFAP)及胶质源性神经营养因子(GDNF)的基因水平明显高于VAD组(P0.05)。结论:VA缺乏抑制HIBD后脑组织功能恢复,推测是VA信号下调GDNF从而抑制NSE、Nestin及GFAP表达,进而影响细胞增殖及功能修复。     

单侧后顶叶皮质过度活动对空间定向功能的影响

摘要 目的：探讨单侧后顶叶皮质的过度活动是否会造成对侧同源脑区的功能抑制并影响空间定向功能。 方法：按照一定的入选标准选取健康受试者30人,采用兴奋性间歇性短阵快速脉冲刺激,随机对左/右侧后顶叶皮质进行真/假刺激,结合注意网络测试系统评定受试者视空间注意功能的变化。 结果：间歇性短阵快速脉冲刺激右侧后顶叶皮质,可以提高警觉及定向功能（P＜0.05）;刺激左侧后顶叶皮质,定向功能受损（P＜0.05）。 结论：右侧后顶叶是空间定向活动的关键脑区,左侧后顶叶过度活动可以导致右侧后顶叶功能抑制。建立双侧半球间新的竞争性平衡,对实现单侧后顶叶损害空间定向功能的康复具有重要意义。     

帕金森病模型大鼠行为学评价与黑质神经元凋亡的相关研究

目的检测帕金森病(PD)模型大鼠行为学及黑质神经元凋亡的相关指标。方法将6-羟基多巴胺(6-OHDA)通过立体定位仪注入大鼠右侧纹状体制备PD模型,5周后检测行为学指标;酪氨酸羟化酶(TH)组化染色观察各组大鼠右侧黑质神经元形态,Hoechst 33258染色了解其凋亡情况,Western blotting方法检测黑质内caspase-3蛋白表达。结果成功筛选的15只PD模型大鼠在露台Morris水迷宫实验中,与正常对照组及假手术组同侧相比,其寻台速度下降,时间延长(P<0-05);在平衡杆实验中,其潜伏期和过杆时间增加(P<0-05);模型组右侧黑质TH阳性神经元明显减少,该区域凋亡细胞明显增多,且caspase-3蛋白表达显著增高。结论6-OHDA诱导黑质内多巴胺(DA)神经元凋亡与其胞内caspase-3表达增高相关,模型大鼠在露台Morris水迷宫和平衡杆实验中行为学改变与TH免疫组化染色及Hoechst 33258染色结果吻合。     

血管性痴呆小鼠海马神经元JNK的表达及意义

目的:探讨血管性痴呆小鼠海马神经元JNK的表达及其意义.方法:应用双侧颈总动脉线结反复缺血一再灌注法制备血管性痴呆小鼠模型,并设正常组、假手术组、血管性痴呆模型组(模型组),利用跳台试验和水迷宫试验观测其行为学改变,应用免疫组化技术观测其海马神经元JNK的表达变化.结果:模型组小鼠与正常组、假手术组相比较,模型组小鼠学习成绩为跳台试验反应时间长,游全程时间长,错误次数多.记忆成绩为跳台试验潜伏时间短,游全程时间长,错误次数多(P＜0.05).海马的JNK免疫反应阳性细胞元免疫组化评分明显增加(P＜0.01).结论:血管性痴呆小鼠认知功能、记忆功能减退与JNK表达增加有关.     

热应激及热应激预处理对小鼠学习记忆以及情绪的影响

目的:从行为学角度研究热应激(HS)及热应激预处理(HP)对小鼠学习记忆及情绪的影响。方法:雄性昆明小鼠32只随机分为对照组、HP组、HS组、(HP+HS)组4组各8只。通过Morris水迷宫评价小鼠学习记忆能力,开场试验评价小鼠自主活动,采用中国地鼠情绪唤醒水平评定量表测定情绪唤醒水平。结果:Morris水迷宫结果显示,与对照组相比,HS组寻找平台潜伏期延长,HP组寻找平台潜伏期缩短,(HP+HS)组寻找平台潜伏期明显缩短,差异具有统计学意义(P0.05);(HP+HS)组与HS组相比,水平运动、垂直运动均有所增多(P0.05);空间搜索试验中,与对照组比较,HS组在目标象限停留的时间明显延长,在目标象限对侧的第三象限停留时间缩短(P0.05);开场试验中,与对照组相比,HS组水平运动、垂直运动、粪便粒数均减少(P0.05),中央格时间延长(P0.05)。结论:HP可使学习记忆能力加强,而急性HS则对学习记忆能力有损害作用,HP可对此损害产生一定保护作用,HS对学习记忆能力的影响随应激后时间推移有减弱趋势。HP使小鼠自主活动增强,急性HS可使自主活动降低。急性HS造成情绪唤醒降低,HP不改变情绪唤醒水平;HS及HP均可降低小鼠的体重。     

足底电击应激对大鼠空间参考记忆维持及海马神经元性一氧化氮合酶表达的影响

目的:观察足底电击应激对大鼠空间参考记忆维持及海马神经元性一氧化氮合酶表达变化的影响。方法:实验于2004-03/2005-03在兰州大学基础医学院解剖教研室完成。健康雄性Wistar大鼠20只,所有大鼠均进行4天Morris水迷宫训练,建立空间记忆模型后随机分为足底电击应激组和鼠笼对照组,每组10只。足底电击应激组每天在8:00～14:00给以足底电击,30V,每30min一次,每次2s,共14d。鼠笼对照组用硬尼龙丝触摸足底,12h内每30min一次,每次2s,共14d。第15天两组大鼠重新进行Morris水迷宫检测,每天训练1次,共训练4d,观察并记录各组大鼠潜伏期、游泳距离、游泳速度、记忆得分。水迷宫实验结束后立即取脑、固定、行冰冻切片(片厚25μm),采用SABC法神经元性一氧化氮合酶免疫组化染色,光镜下进行观察分析、摄像,并记录各组神经元性一氧化氮合酶阳性细胞数。结果:各组大鼠均进入结果分析。①第1次Morris水迷宫实验各指标测试结果:训练至第4天所有大鼠的空间记忆已经形成,4天中游泳速度没有明显的变化。随着训练次数的增加,大鼠空间学习记忆能力逐渐增强。②电击应激后各组大鼠Morris水迷宫实验各指标测试结果:与鼠笼对照组相比,足底电击应激组大鼠游泳距离长、记忆得分低、而游泳速度快,两组比较差异有显著性(P<0.05)。③各组大鼠海马神经元性一氧化氮合酶免疫组化染色结果:足底电击应激组大鼠海马中神经元性一氧化氮合酶免疫反应阳性细胞在CA1、CA2、CA3、CA4及齿状回稀疏,数目较相应鼠笼对照组明显减少(P<0.05)。结论:电击应激可造成大鼠空间参考记忆获得和维持能力的损伤,减少大鼠海马各亚区及齿状回神经元性一氧化氮合酶阳性细胞数。     

Performing allocentric visuospatial judgments with induced distortion of the egocentric reference frame: an fMRI study with clinical implications

The temporary improvement of visuospatial neglect during galvanic vestibular stimulation (Scand. J. Rehabil. Med. 31 (1999)117) may result from correction of the spatial reference frame distorted by the responsible lesion. Prior to an investigation of the neural basis of this effect in neurological patients, exploration of the neural mechanisms underlying such procedures in normals is required to provide insight into the physiological basis thereof. Despite their clinical impact, the neural mechanisms underlying the interaction of galvanic (and other) vestibular manipulations with visuospatial processing (and indeed the neural bases of how spatial reference frames are computed in man) remain to be clarified. We accordingly used fMRI in normal volunteers to investigate the effect of galvanically induced interference with the egocentric spatial reference frame on the neural processes underlying allocentric visuospatial (line bisection) judgments. A significant specific interaction of galvanic vestibular stimulation with the neural mechanisms underlying allocentric visuospatial judgments was observed in right posterior parietal and ventral premotor cortex only. Activation of these areas previously found to be damaged in visuospatial neglect suggests that these effects reflect the increased processing demands when compensating for the distorted egocentric spatial reference frame while maintaining accurate performance during the allocentric spatial task. These results thus implicate right posterior parietal and right ventral premotor cortex in the computation of spatial reference frames. Furthermore, our data imply a specific physiological basis for the temporary improvement of visuospatial neglect in patients with right hemisphere lesions during galvanic vestibular stimulation and may thus impact upon the rehabilitation of neglect: understanding the interaction of galvanic vestibular stimulation with allocentric visuospatial judgments in healthy volunteers may lead to the more effective deployment of such techniques in neurological patients.     

Endogenous and exogenous attention shifts are mediated by the same large-scale neural network

Event-related fMRI was used to examine the neural basis of endogenous (top-down) and exogenous (bottom-up) spatial orienting. Shifts of attention were induced by central (endogenous) or peripheral (exogenous) cues. Reaction times on subsequently presented targets showed the expected pattern of facilitation and inhibition in both conditions. No difference in brain activity was observed when the two orienting conditions were contrasted with a liberal threshold, showing that both forms of orienting were mediated by the same neural network. Compared to within-block control trials, both endogenous and exogenous orienting activated a fronto-parietal network consisting of premotor cortex, posterior parietal cortex, medial frontal cortex and right inferior frontal cortex. Within these regions, equally strong activation was observed for both orienting conditions. It is concluded that endogenous and exogenous orienting are mediated by the same large-scale network of frontal and parietal brain areas.     

Human brain activity related to the perception of spatial features of objects.

The role of the parietal cortex in visuospatial analysis of object was investigated by cerebral blood flow measurements in seven objects using positron emission tomography. Data were acquired while subjects performed a matching task requiring the discrimination of simultaneously presented objects based on one of their spatial properties. Three properties were studied separately during three scanning conditions repeated twice:surface orientation, principal axis orientation, and size. Scans were also obtained during a sensorimotor control task (similar visual stimulation, same motor action, voluntary saccades toward each object) as well as during rest (no stimulation, eyes closed). Compared to rest, the three property matching tasks showed the same pattern of activation: the whole occipital lobe, the right intraparietal sulcus (IPS), and the right occipitotemporal (OT) junction. Compared to the control condition, only right IPS and OT junction were significantly activated during discrimination of the spatial properties. The IPS focus was located between the superior parietal lobule and the angular gyrus, and the OT activation overlapped the posterior part of the inferior temporal gyrus and the middle occipital gyrus. These results indicate that discrimination of spatial attributes requires the activation of both the parietal and the temporal cortices of the right hemisphere and provide further evidence that the IPS plays a critical role in visuospatial analysis of objects.     

阿尔茨海默病模型大鼠感觉门控听觉诱发电位P50诱发电位的变化

背景听觉诱发电位P50为反映大脑正常抑制功能的一种直观的脑电生理学指标.目的观察阿尔茨海默病模型大鼠感觉门控听觉诱发电位P50成分的变化.设计随机对照动物实验.单位昆明医学院神经科学研究所.材料选用雌性健康SD大鼠24只,鼠龄4～6月,体质量200～300 g.按随机抽签法将大鼠分为3组实验组、对照组、正常组,每组8只.Morris水迷宫由圆形水池和有机玻璃站台构成,水池分平台、左、右及对侧4个象限.方法实验于2003-09/2005-03在昆明医学院神经科学研究所完成.①实验组切断双侧穹窿海马伞造成阿尔茨海默病模型;对照组切断皮质、胼胝体,但不切断穹窿海马伞;正常组未手术.②在建模后1周对所有大鼠进行包括检测定位航行能力和空间探索能力的水迷宫试验,以确定造模是否成功;每只大鼠每日训练4次,共训练5 d.入池到找到站台的时间(逃避潜伏期)反映定位航行能力;大鼠1 min内在池中搜索站台的游泳轨迹反映空间探索能力.③采用条件(C)-试验(T)双声刺激模式记录听觉P50诱发电位,比较各组大鼠听觉P50诱发电位的差异.计算C-P50波幅、T-P50波幅、T/C比、S2-S1波幅差的绝对值等.计量资料多组间比较用单因素方差分析,组间比较采用t检验.主要观察指标①各组大鼠水迷宫试验,即定位航行能力和空间探索能力检测结果比较.②各组大鼠感觉门控P50诱发电位比较.结果大鼠24只均进入结果分析.①水迷宫试验结果3组大鼠随着训练天数的增加平均潜伏期缩短,前3 d潜伏期均下降,之后趋平稳.实验组潜伏期明显长于正常组和对照组(P＜0.05).正常组和对照组大鼠的游泳轨迹集中在站台象限,站台象限游泳轨迹分别占总游泳轨迹的45.23%和39.7%,与其他象限间游泳轨迹比较,差异明显(P＜0.01).实验组大鼠在站台、右侧、对侧、左侧象限游泳轨迹占总游泳轨迹的28.31%,29.84%,20.47%和21.38%,差异不明显(P＞0.05),游泳轨迹在4个象限中基本呈随机分布.②大鼠感觉门控P50诱发电位检测结果对照组C-P50波幅和S2-S1波幅差的绝对值分别为(21.00±2.85),(15.26±4.07)μV,正常组分别为(17.04±5.32),(10.85±4.24)μV,明显高于实验组[(9.67±3.77),(2.89±2.61)μV,P＜0.01].对照组和正常组T-P50波幅与C-P50波幅比值分别为0.25±0.18和0.39±0.16,明显低于实验组(0.92±0.41,P＜0.01).结论①用双侧海马伞切断方法可成功制备阿尔茨海默病动物模型.②双侧海马伞切断阿尔茨海默病模型大鼠存在感觉门控能力的不足.     

纳洛酮对东莨菪碱所致大鼠空间工作记忆障碍的干预效应

背景隔-海马区的胆碱能神经通路是空间学习记忆的重要部位,此区神经元中又富含阿片受体.有研究表明阿片类受体拮抗剂纳洛酮能够解除内侧隔区域及海马部位阿片肽对胆碱能神经元活性的抑制,促进突触间隙乙酰胆碱释放,改善空间记忆损害.目的观察阿片类受体拮抗剂纳洛酮对M胆碱能受体阻滞剂东莨菪碱所致大鼠空间工作记忆障碍的干预作用.设计以实验动物为观察对象的随机对照实验.单位佛山市顺德区伍仲珮纪念医院老年科.材料实验于2003-04在汕头大学医学院动物实验中心完成.清洁级SD大鼠21只,随机分成3组,正常组、东莨菪碱组和纳洛酮治疗组(东莨菪碱+纳洛酮),每组7只.自制水迷宫为圆形橡胶水池,直径2 m,高55 cm,水深30 cm,水温20～22℃,在水池东南象限中央放置-圆柱形平台,平台直径12 cm,距水面1.5 cm,此平台为大鼠唯一可逃生之地.池水表面均匀覆以白色聚乙烯碎屑,房内设施如灯管、窗户及桌子等固定,可作为水池外参照目标,水池四壁任意挂置醒目标志数个,可作池内参照目标.方法各组大鼠均于实验前30min腹腔给药,东莨菪碱组(0.4mg/kg),纳洛酮治疗组(3 mg/kg),正常对照组参照东莨菪碱组剂量予等体积生理盐水.然后采用自制水迷宫延缓性匹配任务试验记录每只大鼠前后两次实验逃避潜伏期的时间.于水迷宫测试后迅即处死大鼠,取其左侧大脑组织,常规处理切片.定量测定各组大鼠脑海马和前额叶皮质胆碱乙酰转移酶的表达,采用免疫组化及图像分析技术.同时各组大鼠2只取右侧大脑组织,迅速游离海马,观察大鼠脑海马CA1区的改变,采用电子显微镜技术.所有数据用x±s表示,每组延缓性匹配作业前后两次逃避潜伏期比较采用配对资料t检验;各组间均数比较采用方差分析.以P＜0.05为显著性差异.主要观察指标①各组大鼠前后两次逃避潜伏期结果.②胆碱乙酰转移酶在海马CA1,CA3及前额叶的表达情况.③大鼠海马CA1区超微结构的变化结果21只大鼠全部进入结果分析.①逃避潜伏期的差异前后2次正常组差异有极显著性[(46.4±17.7),(13.4±8.2)s,t=7.32,P＜0.01],东莨菪碱组差异不显著[(23.6±14.3),(18.1±9.8)s,t=1.01,P＞0.05],纳洛酮治疗组差异显著[(27.9±14.3),(9.0±3.8)s,t=3.19,P＜0.05].②胆碱乙酰转移酶的表达正常组、东莨菪碱组、纳洛酮治疗组大鼠的脑海马CA1、CA3区锥体细胞和前额叶皮质神经元的表达无差别(P＞0.05).③大鼠脑海马CA1区超微结构的变化正常组、东莨菪碱组、纳洛酮治疗组大鼠的脑海马CA1区锥体细胞胞体超微结构正常,但神经元突触超微结构发生改变,东莨菪碱组改变明显,突触囊泡明显大小不一,在突触前膜处聚集明显,密度增加,远距离处囊泡大而稀疏分布,突触前后膜模糊,融合,突触间隙不清,突触后致密物质不均、模糊,边界朦胧.结论东莨菪碱组逃避潜伏期观察说明该药能损害大鼠空间工作记忆;纳洛酮能够,促进神经元突触囊泡乙酰胆碱向突触间隙大量释放,增加突触后致密物质密度,解除内侧隔区域及海马部位阿片肽对胆碱能神经元无活性的抑制,具有改善空间记忆损害的作用.     

限食与运动对D-半乳糖诱导的脑老化小鼠的神经保护作用

目的:探讨限食和运动在抗脑老化中的神经保护作用。方法:雄性ICR小鼠60只,随机分为6组,即脑老化模型组(A组)、脑老化模型限食组(B组)、脑老化模型运动组(C组)、运动组(D组)、限食组(E组)和对照组(F组),每组10只,A、B、C组制备脑老化模型,B、E组限食,C、D组运动训练,分别干预10周后,以Morris水迷宫测试小鼠空间记忆和学习能力,以dUTP缺口末端标记(TUNEL)法测定海马神经元凋亡率。结果:A组逃避潜伏期(EL)大于F组(P<0.05),B、C组EL均小于A组(P<0.05)而与F组无差异,D、E组的EL与F组之间无差异;A组海马神经元凋亡率高于F组(P<0.05),B、C组神经元凋亡率低于A组(P<0.05)而与F组之间无差异,D、E组小鼠神经元凋亡率与F组比较亦无差异。结论:限食、运动具有防止脑老化性学习记忆能力下降的效应,并能有效减轻脑老化性神经元凋亡,但对正常小鼠学习记忆能力和神经元凋亡率无明显影响。     

The left parietal and premotor cortices: motor attention and selection

It is well established that the premotor cortex has a central role in the selection of movements. The role of parts of the parietal cortex in movement control has proved more difficult to describe but appears to be related to the preparation and the redirection of movements and movement intentions. We have referred to some of these processes as motor attention. It has been known since the time of William James that covert motor attention can be directed to an upcoming movement just as visuospatial attention can be directed to a location in space. While some parietal regions, particularly in the right hemisphere, are concerned with covert orienting and the redirecting of covert orienting it may be useful to consider other parietal regions, in the anterior inferior parietal lobule and in the posterior superior parietal lobule, particularly in the left hemisphere, as contributing to motor attention. Such parts of the parietal lobe are activated in neuroimaging experiments when subjects covertly prepare movements or switch intended movements. Lesions or transcranial magnetic stimulation (TMS) affect the redirecting of motor attention. The difficulties apraxic patients experience when sequencing movements may partly be due to an inability to redirect motor attention from one movement to another. The role of the premotor cortex in selecting movements is also lateralized to the left hemisphere. Damage to left hemisphere movement selection mechanisms may also contribute to apraxia. If, however, it remains intact after a stroke then the premotor cortex may contribute to the recovery of arm movements. A group of patients with unilateral left hemisphere lesions and impaired movements in the contralateral right hand was studied. Functional magnetic resonance imaging showed that in some cases the premotor cortex in the intact hemisphere was more active when the stroke-affected hand was used. TMS in the same area in the same patients had the most disruptive effect on movements. In summary, patterns of motor impairment and recovery seen after strokes can partly be explained with reference to the roles of the parietal and premotor cortices in motor attention and selection.     

二苯乙烯苷对东莨菪碱致小鼠学习记忆障碍的改善作用

背景中药何首乌能够提高小鼠学习记忆和抗脑缺血能力,而二苯乙烯苷是何首乌的主要有效成份,具有较强的抗氧化与延缓衰老等脑保护作用.目的观察由东莨菪碱所致学习记忆障碍的小鼠给予二苯乙烯苷后,其学习记忆障碍的改善.设计随机对照实验.单位首都医科大学宣武医院药理研究室.材料实验于2000-02/05在首都医科大学宣武医院药物研究中心完成.选取雄性昆明小鼠50只,随机分为5组即正常组、模型组、阳性对照组、二苯乙烯苷0.03g/kg组、二苯乙烯苷0.1g/kg组.二苯乙烯苷为首都医科大学宣武医院药理室从中药何首乌中提取的有效成分,阳性对照药为吡拉西坦,Morris水迷宫和避暗反射箱由中国医学科学院药物研究所研制.方法实验前5d开始给药,正常组及模型组分别给予自来水灌胃,阳性对照组给予吡拉西坦0.7 g/(kg·d),二苯乙烯苷0.03 g/kg组给予二苯乙烯苷0.03 g/(kg·d),二苯乙烯苷0.1 g/kg组给予二苯乙烯苷0.1g/(kg·d),连续5 d.第6天各组灌胃给药30 min后开始造模(正常组腹腔注射等量生理盐水,其余各组均腹腔注射东莨菪碱1 mg/kg),20 min后进行Morris水迷宫和避暗测试.Morris水迷宫造模注射剂量为1 mg/kg,避暗测试造模注射剂量为10 mg/kg.主要观察指标①各组小鼠在Morris水迷宫中的搜索距离和时间.②各组小鼠在避暗实验中的潜伏期和电击次数.结果实验纳入50只小鼠,49只进入结果分析,模型组腹腔注射东莨菪碱时因腹腔出血死亡1只.①Morris水迷宫测试结果二苯乙烯苷0.1 g/kg组小鼠搜索时间及搜索距离较模型组均显著缩短[(77.814±46.492),(99.319±38.104)s;(1370.914±917.40),(1 808.77±869.36)cm;P均＜0.05].②避暗反应测试结果二苯乙烯苷0.03 g/kg与0.1g/kg组小鼠的电击次数较模型组均明显减少[(0.00±0.00),(0.00±0.00),(0.8571±2.267)次,P＜0.01],且潜伏期有延长的趋势[(300±0.00),(300±0.00),(269.71±80.128)S].结论对东莨菪碱所致学习记忆障碍模型小鼠,给予二苯乙烯苷后可缩短其在Morris水迷宫中的搜索时间和搜索距离,减少避暗的错误次数,对学习记忆障碍有一定的改善作用.