CAJ | 학술논문

目的观察FMRI基因敲除型(KO)小鼠脑组织中钙/钙调素依赖蛋白激酶Ⅱα(CaMKⅡα)表达的改变,探讨CaMKⅡα是否为脆性X综合征相关蛋白(FMRP)的下调蛋白. 方法 PCR鉴定FVB近交系小鼠的基因型,按基因型的不同分为KO组和野生型(WT)组,每组10只.免疫组化染色检测KO及WT小鼠脑组织CaMKⅡα的表达与分布,用图像分析仪分别采集不同脑区免疫信号的吸光度(A)值进行比较. 结果免疫组化染色检测显示KO与WT小鼠各个脑区普遍存在阳性信号;神经元胞浆尤其是靠近胞体的近端突起上信号呈强阳性,树突中亦有阳性信号,轴突上信号较弱；KO小鼠各脑区CaMKⅡα阳性信号的A值均较WT小鼠显著增高,差异有统计学意义(P＜0.05). 结论 CaMKⅡα在成年KO小鼠各脑区的表达均显著增多,提示FMRP负性调节CaMKⅡα的表达.
목적 관찰FMRI기인고제형(KO)소서뇌조직중개/개조소의뢰단백격매Ⅱα(CaMKⅡα)표체적개변,탐토CaMKⅡα시부위취성X종합정상관단백(FMRP)적하조단백. 방법 PCR감정FVB근교계소서적기인형,안기인형적불동분위KO조화야생형(WT)조,매조10지.면역조화염색검측KO급WT소서뇌조직CaMKⅡα적표체여분포,용도상분석의분별채집불동뇌구면역신호적흡광도(A)치진행비교. 결과 면역조화염색검측현시KO여WT소서각개뇌구보편존재양성신호;신경원포장우기시고근포체적근단돌기상신호정강양성,수돌중역유양성신호,축돌상신호교약；KO소서각뇌구CaMKⅡα양성신호적A치균교WT소서현저증고,차이유통계학의의(P＜0.05). 결론 CaMKⅡα재성년KO소서각뇌구적표체균현저증다,제시FMRP부성조절CaMKⅡα적표체.
Objective To observe the expression of calcium/calAulin kinaseⅡα (CaMKⅡα) in the brain tissues of fragile X mental retardation 1 (FMR1) gene knockout (KO) mice to investigate whether CaMKⅡα is regulated by fragile X mental retardation protein (FMRP).Methods According to the gene types of the FVB inbred mice identified by PCR,20 mice were divided into KO group and WT (wide type) group (n=10).The subcellular distribution and expression of CaMKⅡα were observed by immunohistochemical staining; the mean optical density (A) values of immunostaining signal of CaMKⅡα in various brain regions,including the motor cortex,temporal cortex,amygdala,hypothalamus and hippocampus,were determined by IBAS 2.0 image-analyzed system.Results CaMKⅡα immunoreactive cells were abundantly found in all brain subregions of KO and WT mice; especial positive signal was noted in the proximal processes of neurons,so as to those in the dendrite; week signcal was observed in the axon.No distributional difference was found between KO and WT mice.As compared with those in the WT mice,the A values were distinctly increased in each brain region of KO mice with significant differences (P＜0.05).Conclusion The increased expression of CaMKⅡα in the brain tissues of FMR1 knockout mice hints that CaMKⅡα participates in the course of the fragile X syndrome,and FMRP may negatively regulate the expression of CaMKⅡα in physiological condition.