Literature DB >> 8088451

Neurites can remain viable after destruction of the neuronal soma by programmed cell death (apoptosis).

T L Deckwerth1, E M Johnson.   

Abstract

During the development of the nervous system extensive programmed neuronal death occurs that is regulated by neurotrophic factors. Invariably, degeneration and death of the neuronal soma as a result of trophic factor deprivation is accompanied by concurrent degeneration of the neurites. By examining the degeneration of sympathetic neurons after deprivation of their physiological trophic factor nerve growth factor, we show that the "slow Wallerian degeneration" allele (Wld6) expressed by homozygous mutant C57BL/Ola mice alters the normal time course of programmed neuronal death by selectively and dramatically delaying the onset of neurite disintegration. In contrast, degenerative events affecting the neuronal soma are not altered: Atrophy of the soma, apoptotic disintegration of the nucleus, commitment to die, and loss of viability occur normally. The enucleate neurites remaining after death of the soma have an intact plasma membrane, are metabolically active, and require an active metabolism for physical integrity. We suggest that the degeneration of neurites during developmentally occurring neuronal death is controlled by events confined to the neurites and occurs autonomously from the neuronal soma. Furthermore, programmed neuronal death of the soma proceeds independent from any influence exerted by degenerating neurites.

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Year:  1994        PMID: 8088451     DOI: 10.1006/dbio.1994.1234

Source DB:  PubMed          Journal:  Dev Biol        ISSN: 0012-1606            Impact factor:   3.582


  57 in total

1.  Evidence that Wallerian degeneration and localized axon degeneration induced by local neurotrophin deprivation do not involve caspases.

Authors:  J T Finn; M Weil; F Archer; R Siman; A Srinivasan; M C Raff
Journal:  J Neurosci       Date:  2000-02-15       Impact factor: 6.167

Review 2.  Wallerian degeneration, wld(s), and nmnat.

Authors:  Michael P Coleman; Marc R Freeman
Journal:  Annu Rev Neurosci       Date:  2010       Impact factor: 12.449

3.  Retrograde and Wallerian axonal degeneration occur synchronously after retinal ganglion cell axotomy.

Authors:  Akiyasu Kanamori; Maria-Magdalena Catrinescu; Jonathan M Belisle; Santiago Costantino; Leonard A Levin
Journal:  Am J Pathol       Date:  2012-05-26       Impact factor: 4.307

Review 4.  Intrinsic axonal degeneration pathways are critical for glaucomatous damage.

Authors:  Gareth R Howell; Ileana Soto; Richard T Libby; Simon W M John
Journal:  Exp Neurol       Date:  2012-01-18       Impact factor: 5.330

Review 5.  Axon pruning: an essential step underlying the developmental plasticity of neuronal connections.

Authors:  Lawrence K Low; Hwai-Jong Cheng
Journal:  Philos Trans R Soc Lond B Biol Sci       Date:  2006-09-29       Impact factor: 6.237

6.  Sensory neuropathy attributable to loss of Bcl-w.

Authors:  Stephanie L Courchesne; Christoph Karch; Maria F Pazyra-Murphy; Rosalind A Segal
Journal:  J Neurosci       Date:  2011-02-02       Impact factor: 6.167

7.  Endogenous Nmnat2 is an essential survival factor for maintenance of healthy axons.

Authors:  Jonathan Gilley; Michael P Coleman
Journal:  PLoS Biol       Date:  2010-01-26       Impact factor: 8.029

8.  Age-dependent synapse withdrawal at axotomised neuromuscular junctions in Wld(s) mutant and Ube4b/Nmnat transgenic mice.

Authors:  Thomas H Gillingwater; Derek Thomson; Till G A Mack; Ellen M Soffin; Richard J Mattison; Michael P Coleman; Richard R Ribchester
Journal:  J Physiol       Date:  2002-09-15       Impact factor: 5.182

9.  Axonal degeneration as a self-destructive defense mechanism against neurotropic virus infection.

Authors:  Ikuo Tsunoda
Journal:  Future Virol       Date:  2008       Impact factor: 1.831

Review 10.  Axon degeneration: context defines distinct pathways.

Authors:  Matthew J Geden; Mohanish Deshmukh
Journal:  Curr Opin Neurobiol       Date:  2016-05-16       Impact factor: 6.627

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