Widespread elimination of naturally occurring neuronal death in Bax-deficient mice

F A White; C R Keller-Peck; C M Knudson; S J Korsmeyer; W D Snider

doi:10.1523/JNEUROSCI.18-04-01428.1998

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Widespread elimination of naturally occurring neuronal death in Bax-deficient mice

Journal article

Open access

Peer reviewed

Widespread elimination of naturally occurring neuronal death in Bax-deficient mice

F A White, C R Keller-Peck, C M Knudson, S J Korsmeyer and W D Snider

The Journal of neuroscience, Vol.18(4), pp.1428-1439

02/15/1998

DOI: 10.1523/JNEUROSCI.18-04-01428.1998

PMID: 9454852

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Abstract

The proapoptotic molecule BAX is required for death of sympathetic and motor neurons in the setting of trophic factor deprivation. Furthermore, adult Bax-/- mice have more motor neurons than do their wild-type counterparts. These findings raise the possibility that BAX regulates naturally occurring cell death during development in many neuronal populations. To test this idea, we assessed apoptosis using TUNEL labeling in several well-studied neural systems during embryonic and early postnatal development in Bax-/- mice. Remarkably, naturally occurring cell death is virtually eliminated between embryonic day 11.5 (E11.5) and postnatal day 1 (PN1) in most peripheral ganglia, in motor pools in the spinal cord, and in the trigeminal brainstem nuclear complex. Additionally, reduction, although not elimination, of cell death was noted throughout the developing cerebellum, in some layers of the retina, and in the hippocampus. Saving of cells was verified by axon counts of dorsal and ventral roots, as well as facial and optic nerves that revealed 24-35% increases in axon number. Interestingly, many of the supernumerary axons had very small cross-sectional areas, suggesting that the associated neurons are not normal. We conclude that BAX is a critical mediator of naturally occurring death of peripheral and CNS neurons during embryonic life. However, rescue from naturally occurring cell death does not imply that the neurons will develop normal functional capabilities.

Neurons - pathology

Brain - embryology

Brain - physiology

Ganglia - physiology

Mice - embryology

Atrophy

Cranial Nerves - physiology

Animals, Newborn - physiology

Neurons - physiology

Cranial Nerves - embryology

Cell Survival - physiology

Ganglia, Spinal - embryology

Neuroglia - physiology

Ganglia, Spinal - physiology

Proto-Oncogene Proteins - deficiency

bcl-2-Associated X Protein

Embryonic and Fetal Development - physiology

Embryo, Mammalian - physiology

Spinal Cord - embryology

Animals

Embryo, Mammalian - cytology

Spinal Cord - physiology

Apoptosis - physiology

Proto-Oncogene Proteins c-bcl-2

Ganglia - embryology

Details

Title: Subtitle: Widespread elimination of naturally occurring neuronal death in Bax-deficient mice
Creators: F A White - Department of Neurology, Center for the Study of Nervous System Injury, Washington University School of Medicine, St. Louis, Missouri 63110, USA
C R Keller-Peck
C M Knudson
S J Korsmeyer
W D Snider
Resource Type: Journal article
Publication Details: The Journal of neuroscience, Vol.18(4), pp.1428-1439
DOI: 10.1523/JNEUROSCI.18-04-01428.1998
PMID: 9454852
NLM abbreviation: J Neurosci
ISSN: 0270-6474
eISSN: 1529-2401
Publisher: United States
Grant note: NS31768 / NINDS NIH HHS P50-AG05681 / NIA NIH HHS HD27500 / NICHD NIH HHS
Language: English
Date published: 02/15/1998
Academic Unit: Pathology; Radiation Oncology
Record Identifier: 9984047685602771

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