GABAB receptor activation protects neurons from apoptosis via IGF-I receptor transactivation
作者单位：Centre National de la Recherche Scientifique（CNRS）Unite Mixte de Recherche 5203Institut de Genomique FonctionnelleMontpellierFrance and INSERMU661MontpellierFrance and Universite Montpellier 12Montpellier F-34000France
会议名称：《中国神经科学学会第四次会员代表大会暨第八届全国学术会议》
会议日期：2009年
学科分类：1001[医学-基础医学(可授医学、理学学位)] 100104[医学-病理学与病理生理学] 10[医学]
关 键 词：GABAB receptor Baclofen apoptosis cerebellum neuroprotection phosphoinositide 3-kinase
摘 要：正The G-protein coupled receptors（GPCRs） and receptor tyrosine kinases（RTKs） play key roles in cell-cell *** studies have revealed important synergisms between these two types of receptors,with some of the actions of either receptor being mediated through transactivation of the *** the large GPCR family,GABAB receptor is activated by the neurotransmitterγ-aminobutyric acid,and is expressed in most neurons where it mediates slow and prolonged inhibition of synaptic *** we show that this receptor is involved in the regulation of life and death decisions of cerebellar granule neurons（CGNs）.We show that specific activation of GABAB receptor can protect neurons from apoptosis through a mechanism that involves transactivation of the IGF-1 *** work demonstrated that this cross-talk was dependent on Gi/o-protein,PLC and PKC,while IGF-1 receptor-induced signaling involved Src kinase,PI3 kinase and Akt *** results reveal a new function for this important GPCR and further highlight the importance of functional cross-talk networks between GPCRs and *** results reveal GABAB receptor as a potential drug target for the treatment of neurodegenerative disorders.