Purpose:To investigate the mechanism of the termination of ocular dominance column plasticity by electrophysiologic analysis and 2-dimensional electrophoresis-mass spectrography(2-DE/MS).Methods:The changes in ocular dominance columns following monocular deprivation were electrophysiologically detected in 22-day-old,100-day-old and chondroitinase-perfused 100-day-old rats.Total protein of grey matter of the primary visual cortex was extracted and studied by 2-DE/MS from the three groups of rats.Results:Monocular deprivation may lead to shifts in ocular dominance columns in 22-day-old and chondroitinase-perfused 100-day-old rats,but not in 100-day-old rats.Four protein spots present in grey matter of the primary visual cortex in 100-day-old,but not in that of 22-day-old and chondroitinase-perfused rats,and mass spectrography identified two of these proteins.Conclusions:The electrophysiologic results show that ocular dominance column plasticity presents in 22-day-old rats,ends up in 100-day-old rats and restored in chondroitinase-perfused 100-day-old rats.2-DE/MS results show that phosphatidylethanolamine binding protein and glial fibrillary acidic protein delta may be associated with the termination of ocular dominance column plasticity in the rat,but need more evidence to confirm it.
目的探索大鼠视皮层中兴奋性神经递质受体表达和分布的发育特征以及双眼形觉剥夺(binocular form deprivation,BFD)对成年大鼠视皮层内兴奋性递质受体亚型表达和分布的影响。方法采用免疫组织化学染色和免疫印迹技术,分别对生后1～9周正常大鼠和自生后7周开始BFD14d后模型大鼠的视皮层中兴奋性递质受体亚型进行标记和检测。结果N-甲基-D-天冬氨酸(N-mehyl-D-aspartate,NMDA)受体亚单位NR2A(NMDA-NR2A)在大鼠未睁眼时少量表达,可塑性关键期高峰时最明显;之后表达减少,至成年期维持一定水平,BFD 14 d可以造成成年大鼠视皮层NM-DA-NR2A阳性表达减弱。NMDA-NR2B在未睁眼时表达较明显,可塑性关键期高峰时表达最多;之后表达下降稳定在成年期低水平,BFD14d可造成其在成年大鼠视皮层中表达增强。α-氨基-3-羟基-5-甲基-4-异唑丙酸受体GluR-1亚基平均分布在视皮层各层,在出生后少量表达,之后随年龄增长逐渐增强,其表达在可塑性关键期终止时达到高峰并在成年期维持较高水平,BFD14d对其在成年大鼠视皮层表达没有影响。结论由BFD诱导的NMDA-NR2A或NMDA-NR2B表达变化可能参与了成年大鼠视皮层可塑性再激活机制。
