CAJ | 학술논문

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,SPSS 11.5统计学软件进行方差分析.结果弱视跟对侧大脑视皮质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mGluR1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人减少致神经元萎缩所致.形觉剥夺致神经冲动传人减少,视皮质17区Ⅳ层mGluR1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.
목적 탐토시각형성관건기내단안형각박탈약시대서초급시피질17구중대사성곡안산수체1(mGluR1)적표체규률급신경원초미결구변화,위림상상게시약시적병리궤제급방치제공의거.방법 수궤대조동기동물실험.방법시건립대서단안형각박탈약시모형,경도형시각유발전위검측증실조모성공후,여정상대조조대서일기관주、고정、취재、주석사절편,진행면역조직화학염색화전경관찰,섭상현미경분층조상,계산궤도상분석계통진행도상분석,SPSS 11.5통계학연건진행방차분석.결과 약시근대측대뇌시피질17구Ⅳ층여정상대조조대뇌시피질17구Ⅳ층화약시안동측대뇌시피질17구Ⅳ층상비,mGluR1양성착색신경원면적감소,차이유통계학의의(P＜0.01).기타각층지간3조분별대비차이균무통계학의의.전경결과현시:약시안대측대뇌시피질17구Ⅳ층가견부분신경원포질경도수종,선립체척화막융합혹소실,배렬문란,조면내질망탈과립현상명현,핵막추축.정상대조조대뇌시피질17구Ⅳ층화약시안동측대뇌시피질17구Ⅳ층신경원포핵정상,핵막완정,선립체척규칙,고이기체발체,조면내질망발체.결론 단안형각박탈약시대뇌시피질17구Ⅳ층mGluR1적표체여정상상비감소.약시안대측대뇌시피질17구Ⅳ층부분신경원발생형태개변,가능여시각신경충동전인감소치신경원위축소치.형각박탈치신경충동전인감소,시피질17구Ⅳ층mGluR1표체감소,돌촉가소성변화,치신경원발생위축가능시약시발병궤제지일.
Objective To explore the regulation of expression of mGluR1 and the changes of neuron ultrastructure 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 resuhs.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 ultrastructure.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.