成年人弱视视皮层可塑性重启以及调节的分子生物学机制

The molecular biological mechanism of restarting and regulating the visual cortex plasticity in adult amblyopia

成年人视皮层可塑性可能与"制动器"、视觉相关信号通路及细胞分子有关。"制动器"通过改变局部及连接之间的神经传递来限制可塑性,阻断这些"制动器"可以促进视皮质锥体细胞树突棘密度恢复、增加神经元树突上的微型兴奋性突触后电流频率和棘突密度、提高视觉诱发电位振幅,以重启成年人视皮层可塑性,治疗弱视。NRG1-ErbB4、PSA-NCAM信号通路异常也改变了神经元形态、结构和功能的可塑性。对细胞因子N-甲基-D-天冬氨酸受体、细胞周期蛋白依赖性激酶5及组蛋白脱乙酰酶的阻断可促进长时程增强现象的发生,调控成年人V1染色质结构和转录,以调节成年人视皮层可塑性重启,治疗弱视。

Adult visual cortex plasticity may be associated with"brakes",visual related signaling pathways and cellular molecules.“Brakes”limit plasticity by altering neural transmission between parts and connections,blocking these"brakes"can promote the recovery of dendritic spines density in pyramidal cells of the visual cortex,increase the frequency of miniature excitatory synaptic current and spinal density on neuron dendrites,and enhance visual evoked potential to reactivate the plasticity in adult visual cortex plasticity and treat amblyopia.The abnormity of NRG1-ErbB4 and PSA-NCAM signaling pathways also change the plasticity,structure and function of neuron morphology.The blocking of N-methyl-D-aspartate-receptor,cyclin-dependent kinase 5 and histone deacetylase can promote long-term potentiation,regulate V1 chromatin structure and transcription in adults to regulate reactivation of visual cortex plasticity in adults.