BAK alters neuronal excitability and can switch from anti- to pro-death function during postnatal development
- BAK alters neuronal excitability and can switch from anti- to pro-death function during postnatal development
- 김종현; Yihru Fannjiang; 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
- Issue Date
- Developmental cell
- VOL 4, NO 4, 575-585
- 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.
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