REGULATION OF ASTROCYTE PROCESSES BY EPHRIN-A3

这个子项目是利用资源的许多研究子项目之一。 由NIH/NCRR资助的中心拨款提供。对子项目的主要支持 子项目的首席调查员可能是由其他来源提供的， 包括美国国立卫生研究院的其他来源。为子项目列出的总成本可能 表示该子项目使用的中心基础设施的估计数量， 不是由NCRR赠款提供给次级项目或次级项目工作人员的直接资金。 神经胶质细胞在神经元的组装和功能中起着关键作用。然而，神经胶质细胞和神经元之间交换的信号并不完全被理解。越来越多的证据支持这一观点，即肾上腺素和Eph受体在神经胶质细胞和神经元轴突以及中枢和外周神经系统不同部分的树突之间的交流中发挥着核心作用。我们之前描述了一种通过EphA4受体酪氨酸激酶及其配体ePhin-A3调节突触后形态的排斥性相互作用。EphA4在成年小鼠海马区锥体神经元的树突棘上有丰富的表达，而EphA3则定位于面对突触的星形细胞突起。我们发现，EphA4被EphA3激活会导致树突棘回缩，而EphA4与EphA4相互作用的减弱会扭曲树突棘的形状和组织。

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. Primary support for the subproject and the subproject's principal investigator may have been provided by other sources, including other NIH sources. The Total Cost listed for the subproject likely represents the estimated amount of Center infrastructure utilized by the subproject, not direct funding provided by the NCRR grant to the subproject or subproject staff. Glial cells play a key role in the assembly and function of neuronal ciruits. However, the signals exchanged by glial cells and neurons are incompletely understood. Increasing evidence supports the notion that ephrins and Eph receptors play a central role in the communication between glial cells and neuronal axons as well as dendrites in different parts of the central and peripheral nervous system. We previously described a repulsive interaction that regulates postsynaptic morphology through the EphA4 receptor tyrosine kinase and its ligand, ephrin-A3. EphA4 is enriched on dendritic spines of pyramidal neurons in the adult mouse hippocampus and ephrin-A3 is localized on astrocytic processes that face synapses. We found that activation of EphA4 by ephrin-A3 induces dendritic spine retraction, whereas decreased EphA4-ephrin interaction distorts dendritic spine shape and organization.