Corticosterone activates Erk1/2 mitogen-activated protein kinase in primary hippocampal cells through rapid nongenomic m
Nongenomic effects of glucocorticoids (GC) in various cell types have been well documented, but it still remains unknown whether the mechanism also works in hippocampus which is a crucial target of glucocorticoids in neural system during physiological and/or pathophysiological processes. We present here that corticosterone (B) could rapidly activate Erk1/2 mitogen-activated protein kinase (MAPK) in primarily cultured hippocampal cells within minutes, with a bell-shaped time dependent curve which peaked at 15min and then went down to normal level in 30 min. This activation was blocked by protein kinase C (PKC) inhibitor (Go6976), G protein inhibitor (GDPβs), and MEK(MAPK/extracellular signal-regulated kinase kinase) inhibitor(PD98059), but not by protein kinase A (PKA) inbibitor (H89), tyrosine kinase inhibitor (genistein), and glucocorticoid receptor ( GR ) antagonist (RU38486). Thus, the rapid activation of Erk1/2 MAPK in primary hippocampal cells induced by B was likely mediated by a G protein coupled receptor (GPCR) pathway with involvement of PKC, which belonged to the nongenomic rather than genomic mechanism of GC' s effects.
作 者： QI Aiqun QIU Jian XIAO Lin CHEN YiZhang 作者单位： QI Aiqun,QIU Jian(Department of Physiology, Second Military Medical University, Shanghai 200433, China)XIAO Lin(Department of Neurobiology, Second Military Medical University, Shanghai 200433, China)
CHEN YiZhang(Department of Neurobiology, Second Military Medical University, Shanghai 200433, China;Institute of Neuroscience, Second Military Medical University, Shanghai 200433, China)
刊 名： 自然科学进展（英文版） SCI 英文刊名： PROGRESS IN NATURAL SCIENCE 年，卷(期)： 2005 15(4) 分类号： Q5 关键词： glucocorticoid MAPK rapid effects nongenomic mechanism