蛋白激酶α和β在视觉剥夺性大鼠视皮层中表达变化的初步研究

目的　检测蛋白激酶α和 β(PKCα、PKCβ)在正常大鼠视皮层及视觉剥夺性视皮层中的蛋白表达情况 ,为探讨视觉发育可塑性提供分子基础。方法　采用剥夺性弱视大鼠模型 ,用特异的PKCα和PKCβ抗体对脑切片进行免疫组化。 结果　正常视皮层中 ,这两种PKC同工酶在除Ⅰ层外的其余各层均有显著表达。视觉剥夺的视皮层缺乏正常视皮层那样的清晰分层。与正常视皮层比较 ,弱视眼对侧视皮层中PKCα在Ⅱ～Ⅳ层的蛋白表达广泛减少 ,PKCβ在Ⅱ～Ⅴ层的表达强度明显减弱。结论　PKCα、PKCβ的蛋白表达水平在剥夺性视皮层发育障碍过程中发生了显著改变 ,它们可能参与视皮层发育可塑性的分子机制。

Primary report for investigation of changes in the expressions for PKCα and PKCβ isozymes in visual cortex of deprived rat

Objective To identify the protein expressions for protein kinase C alpha and protein kinase C beta isozymes in visual cortex of normal rat or deprived rat by one eyelid sutuered closed, providing the molecular basis to investigate the plasticity of visual development.Methods Classical model of deprived amblyopia rat was employed.Immunohistochemistry was performed using specific antibody against PKCalpha or PKCbeta isozyme, respectively.Results Prominent signals for protein kinase Calpha and protein kinase Cbeta isozymes were distributed throughout layer Ⅱ～Ⅵ of normal visual cortex. Layer specific expression pattern in normal visual cortex was found lost in the deprived visual cortex. Compared with protein expression in normal visual cortex, the PKCalpha isozyme was weakly expressed at low level throughout layer Ⅱ～Ⅳ in deprived visual cortex. PKCbeta was detected weak signals in layer Ⅱ～Ⅴ.Conclusion There were notable changes in expression level of PKCalpha and beta proteins during the deranged development of deprived visual cortex. Our results suggest that PKCalpha and PKCbeta may be involved in the molecular mechanism which governs the plasticity of visual development.