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

doi:10.1016/S1534-5807(03)00091-1

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

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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 language	English (US)
Pages (from-to)	575-585
Number of pages	11
Journal	Developmental Cell
Volume	4
Issue number	4
DOIs	https://doi.org/10.1016/S1534-5807(03)00091-1
State	Published - Apr 1 2003

ASJC Scopus subject areas

Molecular Biology
General Biochemistry, Genetics and Molecular Biology
Developmental Biology
Cell Biology

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Fannjiang, Y., Kim, C. H., Huganir, R. L., Zou, S., Lindsten, T., Thompson, C. B., Mito, T., Traystman, R. J., Larsen, T., Griffin, D. E., Mandir, A. S., Dawson, T. M., Dike, S., Sappington, A. L., Kerr, D. A., Jonas, E. A., Kaczmarek, L. K., & Hardwick, J. M. (2003). BAK alters neuronal excitability and can switch from anti- to pro-death function during postnatal development. Developmental Cell, 4(4), 575-585. https://doi.org/10.1016/S1534-5807(03)00091-1

Fannjiang, Y, Kim, CH, Huganir, RL, Zou, S, Lindsten, T, Thompson, CB, Mito, T, Traystman, RJ, Larsen, T, Griffin, DE, 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

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

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.",

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

note = "Funding Information: This work was supported by grants from the National Institutes of Health to J.M.H. (NS34175 and NS37402), R.L.H., C.B.T., R.J.T. (NS20020), D.E.G. (NS18597), T.M.D. (NS38377 and NS43691), D.A.K. (NS02130), L.K.K. (DC01919 and NS01849), and from the American Federation for Aging Research to A.S.M.",

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AU - Fannjiang, Yihru

AU - Kim, Chong Hyun

AU - Huganir, Richard L.

AU - Zou, Shifa

AU - Lindsten, Tullia

AU - Thompson, Craig B.

AU - Mito, Toshiaki

AU - Traystman, Richard J.

AU - Larsen, Thomas

AU - Griffin, Diane E.

AU - Mandir, Allen S.

AU - Dawson, Ted M.

AU - Dike, Sonny

AU - Sappington, Andrea L.

AU - Kerr, Douglas A.

AU - Jonas, Elizabeth A.

AU - Kaczmarek, Leonard K.

AU - Hardwick, J. Marie

N1 - Funding Information: This work was supported by grants from the National Institutes of Health to J.M.H. (NS34175 and NS37402), R.L.H., C.B.T., R.J.T. (NS20020), D.E.G. (NS18597), T.M.D. (NS38377 and NS43691), D.A.K. (NS02130), L.K.K. (DC01919 and NS01849), and from the American Federation for Aging Research to A.S.M.

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N2 - 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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BAK alters neuronal excitability and can switch from anti- to pro-death function during postnatal development

Abstract

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