中国现代医学杂志
中國現代醫學雜誌
중국현대의학잡지
CHINA JOURNAL OF MODERN MEDICINE
2004年
11期
26-30,34
,共6页
刘正清%马志健%李明波%蔡维君%王春旭%文晓丹
劉正清%馬誌健%李明波%蔡維君%王春旭%文曉丹
류정청%마지건%리명파%채유군%왕춘욱%문효단
血管性痴呆,Morris水迷宫%微管相关蛋白-2%神经丝蛋白
血管性癡呆,Morris水迷宮%微管相關蛋白-2%神經絲蛋白
혈관성치태,Morris수미궁%미관상관단백-2%신경사단백
vascular dementia%global cerebral isehemia and reporfusion%morris water maze%MAP-2%NF
目的观察血管性痴呆大鼠海马CAI区神经元MAP-2、NF表达变化,探讨缺血再灌注损伤后神经元骨架蛋白表达变化与学习记忆的相互关系.方法采用Morris水迷宫筛选空间学习记忆能力正常的雄性Wistar大鼠60只;正常组(Norma1);椎动脉焊扎组(VO);双侧颈总动脉结扎20 nin再灌组(BCCO/R);全脑缺血20min再灌组(GI/R);后三组又分为存活7,14和30天组,处死前作水迷宫检测.用免疫组织化学方法检测MAP-2和NF表达,常规尼氏染色法镜下计数海马CAI区存活神经元.结果水迷宫检测GI/R组大鼠潜伏期增加,尼氏染色证实GI/R组锥体神经元减少(P<0.01).与Normal组比较,BCCO/R7 d组海马CAI区辐射层MAP-2表达减弱,神经元突起中NF表达减少(P<0.05);而BCCO/R14 d和3O d组胞浆MAP--2和NF表达均无变化(P>0.05).GI/R组海马CAI区MAP-2、NF的表达在突起中几乎消失,而在锥体神经元核周有强表达,与各对照组比较判别有统计学意义(P<0.05).结论MAP-2、NF在神经元突起中减少,而在胞体中聚集,是神经元可塑性的体现,在血管性痴呆动物模型中,可能对神经元有保护作用.
目的觀察血管性癡呆大鼠海馬CAI區神經元MAP-2、NF錶達變化,探討缺血再灌註損傷後神經元骨架蛋白錶達變化與學習記憶的相互關繫.方法採用Morris水迷宮篩選空間學習記憶能力正常的雄性Wistar大鼠60隻;正常組(Norma1);椎動脈銲扎組(VO);雙側頸總動脈結扎20 nin再灌組(BCCO/R);全腦缺血20min再灌組(GI/R);後三組又分為存活7,14和30天組,處死前作水迷宮檢測.用免疫組織化學方法檢測MAP-2和NF錶達,常規尼氏染色法鏡下計數海馬CAI區存活神經元.結果水迷宮檢測GI/R組大鼠潛伏期增加,尼氏染色證實GI/R組錐體神經元減少(P<0.01).與Normal組比較,BCCO/R7 d組海馬CAI區輻射層MAP-2錶達減弱,神經元突起中NF錶達減少(P<0.05);而BCCO/R14 d和3O d組胞漿MAP--2和NF錶達均無變化(P>0.05).GI/R組海馬CAI區MAP-2、NF的錶達在突起中幾乎消失,而在錐體神經元覈週有彊錶達,與各對照組比較判彆有統計學意義(P<0.05).結論MAP-2、NF在神經元突起中減少,而在胞體中聚集,是神經元可塑性的體現,在血管性癡呆動物模型中,可能對神經元有保護作用.
목적관찰혈관성치태대서해마CAI구신경원MAP-2、NF표체변화,탐토결혈재관주손상후신경원골가단백표체변화여학습기억적상호관계.방법채용Morris수미궁사선공간학습기억능력정상적웅성Wistar대서60지;정상조(Norma1);추동맥한찰조(VO);쌍측경총동맥결찰20 nin재관조(BCCO/R);전뇌결혈20min재관조(GI/R);후삼조우분위존활7,14화30천조,처사전작수미궁검측.용면역조직화학방법검측MAP-2화NF표체,상규니씨염색법경하계수해마CAI구존활신경원.결과수미궁검측GI/R조대서잠복기증가,니씨염색증실GI/R조추체신경원감소(P<0.01).여Normal조비교,BCCO/R7 d조해마CAI구복사층MAP-2표체감약,신경원돌기중NF표체감소(P<0.05);이BCCO/R14 d화3O d조포장MAP--2화NF표체균무변화(P>0.05).GI/R조해마CAI구MAP-2、NF적표체재돌기중궤호소실,이재추체신경원핵주유강표체,여각대조조비교판별유통계학의의(P<0.05).결론MAP-2、NF재신경원돌기중감소,이재포체중취집,시신경원가소성적체현,재혈관성치태동물모형중,가능대신경원유보호작용.
Objective:To investigate the expression of MAP-2 and NF in CA1 region of hippocampal neurons and its relation with spatial learning and memory in vascular dementia model(VD).Methods:60Wistar rats with normal learning and memory confirmed by Morris water maze were divided into 4 groups group(GI/R).According to animal surviving period,the last three groups were subdivided into three groups,7,14 and 30days.These rats were tested again in Morris water maze before being sacrificed.Expression of MAP-2 and NF were detected by immunohistochemistry and the intensity of immunostaining was measured by MedHPIAS pathologic imaging-analysis system.Coronal slices with Nissl's staining were used to count neurons in hippocampus CAI regions.Results:Compared with groups normal,VO and BCCO/R,escape latency of GI/R group was longer following elongation of reperfusion(P<0.01).In Hippocampus CA1 regions the number of neurons was not reduced in groups VO and BCCO/R,but decreased in GI/R groups(P<0.01),and had significant differences among the GI/R 7,14 and 30d groups(P<0.01).Compared with normal group,expressions of MAP-2 and NF in Hippocampus CAI region obviously reduced in BCCO/R7d group(P<0.05),but in groups BCCO/R 14 d and 30 d their expressions had no significant change(P>0.05).In groups GI/R the neurites with immunostaining of MAP-2 and NF were not observed,but strong staining of these two proteins was present in perikaryon of the neurons(P<0.O5).Conclusions:The expression pattern of MAP-2 and NF indicates that neuronal plasticity is the responding to injury.The finding that MAP-2 and NF were aggregated in cytoplasm might imply their protective roles to neuron in vascular dementia.