早期应激诱导神经元树突棘形态结构重塑研究进展  

Research progress of morphological remodeling of neuronal dendritic spine induced by early stress

作　　者：何云[1] 杨群[1] 许本柯[1] 

机构地区：[1]长江大学医学院解剖教研室,荆州434023

出　　处：《新医学》2015年第5期279-282,共4页Journal of New Medicine

摘　　要：生长发育早期,促肾上腺皮质激素释放因子(CRF)可导致海马神经元突触功能发生改变,神经元树突棘形态结构重塑,最终损害海马记忆功能。CRFR1受体广泛存在于海马神经元树突棘头部突触后致密物(PSD)上,CRF与CRFR1受体结合,可通过G蛋白偶联受体介导的信号转导调控神经元突触相关功能,此外还可通过激活Rho A-confilin网络信号导致神经元树突棘形态结构发生改变。该文就树突棘形态结构、分子组成及相关调节蛋白以及CRF与海马相应功能区神经元树突棘作用等内容作一综述。During the early stage of growth and development,corticotropin releasing factors （CRF） can alter the function of synapse of hippocampal neurons,remodel the morphology of neuronal dendritic spine and eventually damage the memory function of hippocampus.CRFR1 receptor is widely distributed in the posts-ynaptic dense materials （PSD）of dendritic spine head of hippocampal neurons.Binding of CRF and CRFR1 receptors not only could regulate the function of neuronal synapse via G-protein coupling receptor-mediated sig-naling transduction,but also cause morphological variations of neuronal dendritic spine through activating RhoA-confilin signaling network.This paper summarized the morphology,molecular composition and related regulatory proteins of dendritic spine and the effect of CRF upon neuronal dendritic spine in the corresponding domain of hippocampus,etc.

关 键 词：应激 树突棘 突触 促肾上腺皮质激素释放因子 海马 

分 类 号：R741[医药卫生—神经病学与精神病学]