Corticosterone activates Erk1/2 mitogen-activated protein kinase in primary hippocampal cells through rapid nongenomic mechanism

Aiqun Qi, Jian Qiu, Lin Xiao, Yizhang Chen

Research output: Contribution to journalArticlepeer-review

Abstract

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.

Original languageEnglish (US)
Pages (from-to)325-330
Number of pages6
JournalProgress in Natural Science
Volume15
Issue number4
StatePublished - Apr 1 2005
Externally publishedYes

Keywords

  • Glucocorticoid
  • MAPK
  • Nongenomic mechanism.
  • Rapid effects

ASJC Scopus subject areas

  • Materials Science(all)

Fingerprint

Dive into the research topics of 'Corticosterone activates Erk1/2 mitogen-activated protein kinase in primary hippocampal cells through rapid nongenomic mechanism'. Together they form a unique fingerprint.

Cite this