PirB通过突触可塑性介导学习记忆的调控作用

Regulation of learning and memory through synaptic plasticity mediated by PirB

成对免疫球蛋白样受体B(paired immunoglobulin-like receptor B,PirB)作为中枢微环境中的髓鞘相关抑制因子及主要组织相容性复合体I的共同受体,在中枢神经系统损伤后可抑制轴突再生,且对突触可塑性具有明显的调节作用。在正常情况下,PirB参与的抑制信号有助于平衡学习和记忆等基本大脑功能所需的稳态,而在损伤状态下这种抑制效应则会影响突触可塑性,导致神经元回路的永久性损伤。综述了PirB的生物学功能并在此基础上深入探讨了PirB介导突触可塑性调控学习记忆的作用机制,为认知及精神障碍类疾病的预防与治疗提供了理论依据。

The paired immunoglobulin-like receptor B(PirB),as the co-receptor of myelin-associated inhibitors(MAIs)and major histocompatibility complex I(Class I)in the central microenvironment,inhibits axon regeneration after central nervous system injury,and also has a regulatory effect on synaptic plasticity.In a healthy central nervous system,the inhibitory signal mediated by PirB helps balance homeostasis required for basic brain functions such as learning and memory.However,upon injury this inhibition affects synaptic plasticity,resulting in permanent damage to neuronal circuits.This article reviews the biological functions of PirB,and further discusses the mechanism of PirB mediated synaptic plasticity in regulating learning and memory,which may provide a theoretical basis for the prevention and treatment of cognitive and mental disorders.