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作 者:王宗青[1] 刘向玲[2] 穆雅林 刘爱琴[2] 李晓鹏[2]
机构地区:[1]河南省三门峡市黄河三门峡医院眼科,472000 [2]新乡医学院第三附属医院眼科
出 处:《中华眼科杂志》2008年第1期67-71,共5页Chinese Journal of Ophthalmology
摘 要:目的探讨视觉形成关键期内单眼形觉剥夺弱视大鼠初级视皮质17区中代谢性谷氨酸受体1(mGluR1)的表达规律及神经元超微结构变化,为临床上揭示弱视的病理机制及防治提供依据。方法随机对照同期动物实验。方法是建立大鼠单眼形觉剥夺弱视模型,经图形视觉诱发电位检测证实造模成功后,与正常对照组大鼠一起灌注、固定、取材、做石蜡切片,进行免疫组织化学染色和电镜观察,摄像显微镜分层照相,计算机图像分析系统进行图像分析,SPSS11.5统计学软件进行方差分析。结果弱视眼对侧大脑视皮质17区Ⅳ层与正常对照组大脑视皮质17区Ⅳ层和弱视眼同侧大脑视皮质17区Ⅳ层相比,mGluR1阳性着色神经元面积减少,差异有统计学意义(P〈0.01)。其他各层之间3组分别对比差异均无统计学意义。电镜结果显示:弱视眼对侧大脑视皮质17区Ⅳ层可见部分神经元胞质轻度水肿,线粒体嵴和膜融合或消失,排列紊乱,粗面内质网脱颗粒显像明显,核膜皱缩。正常对照组大脑视皮质17区Ⅳ层和弱视眼同侧大脑视皮质17区Ⅳ层神经元胞核正常,核膜完整,线粒体嵴规则,高尔基体发达,粗面内质网发达。结论单眼形觉剥夺弱视大脑视皮质17区Ⅳ层mGluR,的表达与正常相比减少。弱视眼对侧大脑视皮质17区Ⅳ层部分神经元发生形态改变,可能与视觉神经冲动传入减少致神经元萎缩所致。形觉剥夺致神经冲动传入减少,视皮质17区Ⅳ层mGluR,表达减少,突触可塑性变化,致神经元发生萎缩可能是弱视发病机制之一。(中华眼科杂志,2008,44:67—71)Objective To explore the regulation of expression of mGluRl and the changes of neuron uhrastructure at primary visual cortex of monocular deprivation amblyopia rat within cortical period. Methods Taking randomized concurrent controlled trail. Establishing the model of monocular deprivation amblyopia rat. After proving the model successful by PVEP, all of the rats were randomly divided into three groups: normal visual cortex, experimental visual cortex and experimental opposite visual cortex. Immunocytochemical technology, electron microscope, photography microscope, computer image analysis, SPSS 11.5 and ANOV were used to get the results. Results Compared with the layer IV of normal visual cortex and experimental opposite visual cortex, the area of immunopositive neurons in layer IV of experimental visual cortex are deficiency, there is significant difference between them ( P 〈 0.01 ). There are no significant differences between the other four corresponding layers ( P 〉 0.05 ). Morphological abnormals were found in layer IV of experimental visual cortex by observing of uhrastructure. Conclusion The expression of mGluR1 in layer IV of primary visual cortex of monocular deprivation amblyopia is reduced. There are morphological abnormals happened in layer IV of primary visual cortex of monocular derivation amblyopia. Reduced afference of nerve pulse because of monocular deprivation leads to the expression difficiency of mGluR1 in layer IV of the primary visual cortex, then synaptic plasticity happened, then neurons atrophy occurred may be one of the etiopathogenesis of amblyopia. (Chin J Ophthalmol, 2008,44: 67-71 )
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