CaMKII in cerebral ischemia

Steven J. Coultrap, Rebekah S. Vest, Nicole M. Ashpole, Andy Hudmon, K. Ulrich Bayer

Research output: Contribution to journalReview articlepeer-review

60 Scopus citations


Ischemic insults on neurons trigger excessive, pathological glutamate release that causes Ca 2+ overload resulting in neuronal cell death (excitotoxicity). The Ca 2+ /calmodulin (CaM)-dependent protein kinase II (CaMKII) is a major mediator of physiological excitatory glutamate signals underlying neuronal plasticity and learning. Glutamate stimuli trigger autophosphorylation of CaMKII at T286, a process that makes the kinase autonomous (partially active independent from Ca 2+ stimulation) and that is required for forms of synaptic plasticity. Recent studies suggested autonomous CaMKII activity also as potential drug target for post-insult neuroprotection, both after glutamate insults in neuronal cultures and after focal cerebral ischemia in vivo. However, CaMKII and other members of the CaM kinase family have been implicated in regulation of both neuronal death and survival. Here, we discuss past findings and possible mechanisms of CaM kinase functions in excitotoxicity and cerebral ischemia, with a focus on CaMKII and its regulation.

Original languageEnglish (US)
Pages (from-to)861-872
Number of pages12
JournalActa Pharmacologica Sinica
Issue number7
StatePublished - Jul 2011


  • brain ischemia
  • CaM kinases
  • CaMKII
  • excitotoxicity
  • glutamate
  • stroke

ASJC Scopus subject areas

  • Pharmacology
  • Pharmacology (medical)

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