Ether stress-induced Alzheimer-like tau phosphorylation in the normal mouse brain

FEBS Lett. 2007 Mar 6;581(5):891-7. doi: 10.1016/j.febslet.2007.01.064. Epub 2007 Feb 2.

Abstract

Tau is reversibly hyperphosphorylated in the mouse brain by starvation or cold water swimming. Here, we report tau phosphorylation in the hippocampus of normal mouse after ether anesthesia, known to trigger typical stress reactions. Robust phosphorylation of tau was observed immediately and 10min after ether vapor exposure at Ser202/Thr205 and Thr231/Ser235, sites typically phosphorylated in Alzheimer brains. The phosphorylation levels returned to baseline by 1h. The most conspicuous and consistent change in the protein kinases studied was the inactivating phosphorylation of Ser9 of TPKI/GSK3beta in close correspondence with tau phosphorylation. These findings show that tau phosphorylation is a rapid physiological process integral to stress response system, and suggest involvement therein of TPKI/GSK3beta.

MeSH terms

  • Alzheimer Disease / metabolism
  • Animals
  • Binding Sites
  • Brain / drug effects*
  • Brain / metabolism*
  • Ether / toxicity*
  • Glycogen Synthase Kinase 3 / metabolism
  • Glycogen Synthase Kinase 3 beta
  • Hippocampus / drug effects
  • Hippocampus / metabolism
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Phosphorylation
  • Protein Serine-Threonine Kinases / metabolism
  • Stress, Physiological / metabolism
  • tau Proteins / chemistry
  • tau Proteins / metabolism*

Substances

  • tau Proteins
  • Ether
  • Glycogen Synthase Kinase 3 beta
  • Gsk3b protein, mouse
  • Protein Serine-Threonine Kinases
  • Glycogen Synthase Kinase 3
  • tau-protein kinase