Eph Receptors and Ephrins in Neuron-Astrocyte Communication at Synapses  被引量:3

Eph Receptors and Ephrins in Neuron-Astrocyte Communication at Synapses

在线阅读下载全文

作  者:Murai KK Pasquale EB 

机构地区:[1]Centre for Research in Neuroscience,Department of Neurology and Neurosurgery,McGill University Health Centre [2]anford-Burnham Medical Research Institute,La Jolla,California [3]Pathology Department,University of California,San Diego,Californi

出  处:《神经损伤与功能重建》2011年第6期440-450,共11页Neural Injury and Functional Reconstruction

摘  要:神经元-胶质细胞间的相互作用对调节脑内突触联系有重要作用。星形胶质细胞对突触的发育、维持和可塑性有特别关键、复杂的作用。同样,神经元也对星形胶质细胞的生理功能产生影响。但是,神经元和星形胶质细胞之间相互作用的分子机制尚未完全阐明。近来研究表明,Eph受体酪氨酸激酶及轴突导向因子在突触间接触依赖性神经元-胶质细胞的相互作用中起重要作用。与配体结合后,这2个细胞表面相关蛋白家族成员激活双向信号通路,调节神经元和星形胶质细胞的结构和生理特征。本综述着重探讨Eph受体酪氨酸激酶及轴突导向因子在突触间神经元-胶质细胞的相互作用中扮演的角色,并讨论其在突触可塑性、行为及疾病中的潜在作用。Neuron-glia communication is essential for regulating the properties of synaptic connections in the brain. Astrocytes, in particular, play a critical and complex role in synapse development, maintenance, and plastici- ty. Likewise, neurons reciprocally influence astrocyte physiology. However, the molecular signaling events that en- able astrocytes and neurons to effectively communicate with each other are only partially defined. Recent findings have revealed that Eph receptor tyrosine kinases and ephrins play an important role in contact-dependent neuron-glia communication at synapses. Upon binding, these two families of cell surface-associated proteins trigger bidirectional signaling events that regulate the structural and physiological properties of both neurons and astrocytes. This review will focus on the emerging role of Eph receptors and ephrins in neuron-astrocyte interaction at synapses and discuss implications for synaptic plasticity, behavior, and disease. @ 2010 Wiley-Liss, Inc.

关 键 词:胶质细胞 信号 树突 谷氨酸转运体 可塑性 海马 

分 类 号:R741[医药卫生—神经病学与精神病学]

 

参考文献:

正在载入数据...

 

二级参考文献:

正在载入数据...

 

耦合文献:

正在载入数据...

 

引证文献:

正在载入数据...

 

二级引证文献:

正在载入数据...

 

同被引文献:

正在载入数据...

 

相关期刊文献:

正在载入数据...

相关的主题
相关的作者对象
相关的机构对象