BAK alters neuronal excitability and can switch from anti- to pro-death function during postnatal development

Yihru Fannjiang, Chong Hyun Kim, Richard L. Huganir, Shifa Zou, Tullia Lindsten, Craig B. Thompson, Toshiaki Mito, Richard J. Traystman, Thomas Larsen, Diane E. Griffin, Allen S. Mandir, Ted M. Dawson, Sonny Dike, Andrea L. Sappington, Douglas A. Kerr, Elizabeth A. Jonas, Leonard K. Kaczmarek, J. Marie Hardwick

Research output: Contribution to journalArticlepeer-review


BAK is a pro-apoptotic BCL-2 family protein that localizes to mitochondria. Here we evaluate the function of BAK in several mouse models of neuronal injury including neuronotropic Sindbis virus infection, Parkinson's disease, ischemia/stroke, and seizure. BAK promotes or inhibits neuronal death depending on the specific death stimulus, neuron subtype, and stage of postnatal development. BAK protects neurons from excitotoxicity and virus infection in the hippocampus. As mice mature, BAK is converted from anti- to pro-death function in virus-infected spinal cord neurons. In addition to regulating cell death, BAK also protects mice from kainate-induced seizures, suggesting a possible role in regulating synaptic activity. BAK can alter neurotransmitter release in a direction consistent with its protective effects on neurons and mice. These findings suggest that BAK inhibits cell death by modifying neuronal excitability.

Original languageEnglish (US)
Pages (from-to)575-585
Number of pages11
JournalDevelopmental Cell
Issue number4
StatePublished - Apr 1 2003

ASJC Scopus subject areas

  • Molecular Biology
  • Biochemistry, Genetics and Molecular Biology(all)
  • Developmental Biology
  • Cell Biology


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