Hypothermia treatment potentiates ERK1/2 activation after traumatic brain injury

Coleen M. Atkins, Anthony A. Oliva, Ofelia F. Alonso, Shaoyi Chen, Helen M. Bramlett, Bing Ren Hu, W. Dalton Dietrich

Research output: Contribution to journalArticlepeer-review

46 Scopus citations


Traumatic brain injury (TBI) results in significant hippocampal pathology and hippocampal-dependent memory loss, both of which are alleviated by hypothermia treatment. To elucidate the molecular mechanisms regulated by hypothermia after TBI, rats underwent moderate parasagittal fluid-percussion brain injury. Brain temperature was maintained at normothermic or hypothermic temperatures for 30 min prior and up to 4 h after TBI. The ipsilateral hippocampus was assayed with Western blotting. We found that hypothermia potentiated extracellular signal-regulated kinase 1/2 (ERK1/2) activation and its downstream effectors, p90 ribosomal S6 kinase (p90RSK) and the transcription factor cAMP response element-binding protein. Phosphorylation of another p90RSK substrate, Bad, also increased with hypothermia after TBI. ERK1/2 regulates mRNA translation through phosphorylation of mitogen-activated protein kinase-interacting kinase 1 (Mnk1) and the translation factor eukaryotic initiation factor 4E (eIF4E). Hypothermia also potentiated the phosphorylation of both Mnk1 and eIF4E. Augmentation of ERK1/2 activation and its downstream signalling components may be one molecular mechanism that hypothermia treatment elicits to improve functional outcome after TBI.

Original languageEnglish (US)
Pages (from-to)810-819
Number of pages10
JournalEuropean Journal of Neuroscience
Issue number4
StatePublished - Aug 2007


  • CREB
  • ERK1/2
  • Fluid-percussion
  • Hypothermia
  • Traumatic brain injury

ASJC Scopus subject areas

  • Neuroscience(all)


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