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 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 journalArticle

Abstract

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
Volume4
Issue number4
DOIs
StatePublished - Apr 1 2003

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Neurons
Viruses
Switches
Cell death
Virus Diseases
Seizures
Cell Death
Sindbis Virus
Mitochondria
Kainic Acid
Neurotransmitter Agents
Parkinson Disease
Hippocampus
Spinal Cord
Ischemia
Stroke
Wounds and Injuries
Proteins

ASJC Scopus subject areas

  • Developmental Biology

Cite this

BAK alters neuronal excitability and can switch from anti- to pro-death function during postnatal development. / Fannjiang, Yihru; Kim, Chong Hyun; Huganir, Richard L; Zou, Shifa; Lindsten, Tullia; Thompson, Craig B.; Mito, Toshiaki; Traystman, Richard J.; Larsen, Thomas; Griffin, Diane; Mandir, Allen S.; Dawson, Ted M; Dike, Sonny; Sappington, Andrea L.; Kerr, Douglas A.; Jonas, Elizabeth A.; Kaczmarek, Leonard K.; Hardwick, J Marie.

In: Developmental Cell, Vol. 4, No. 4, 01.04.2003, p. 575-585.

Research output: Contribution to journalArticle

Fannjiang, Y, Kim, CH, Huganir, RL, Zou, S, Lindsten, T, Thompson, CB, Mito, T, Traystman, RJ, Larsen, T, Griffin, D, Mandir, AS, Dawson, TM, Dike, S, Sappington, AL, Kerr, DA, Jonas, EA, Kaczmarek, LK & Hardwick, JM 2003, 'BAK alters neuronal excitability and can switch from anti- to pro-death function during postnatal development', Developmental Cell, vol. 4, no. 4, pp. 575-585. https://doi.org/10.1016/S1534-5807(03)00091-1
Fannjiang, Yihru ; Kim, Chong Hyun ; Huganir, Richard L ; Zou, Shifa ; Lindsten, Tullia ; Thompson, Craig B. ; Mito, Toshiaki ; Traystman, Richard J. ; Larsen, Thomas ; Griffin, Diane ; Mandir, Allen S. ; Dawson, Ted M ; Dike, Sonny ; Sappington, Andrea L. ; Kerr, Douglas A. ; Jonas, Elizabeth A. ; Kaczmarek, Leonard K. ; Hardwick, J Marie. / BAK alters neuronal excitability and can switch from anti- to pro-death function during postnatal development. In: Developmental Cell. 2003 ; Vol. 4, No. 4. pp. 575-585.
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