ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2003
Neuromuscular development after the prevention of naturally occurring neuronal death by Bax deletion.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
32 citing papers in PubMed, 67 citations in OpenAlex.
- Autophagy and apoptosis cascade: which is more prominent in neuronal death?Cellular and molecular life sciences : CMLS · 2021Review
- The role of Bcl-2 proteins in modulating neuronal CaBiochimica et biophysica acta. Molecular cell research · 2021Review
- Neuronal cell life, death, and axonal degeneration as regulated by the BCL-2 family proteins.Cell death and differentiation · 2021Review
- Cell death in animal development.Development (Cambridge, England) · 2020Review
- The essentials of developmental apoptosis.F1000Research · 2020Review
- Non-apoptotic cell death in animal development.Cell death and differentiation · 2017Review
- Patterns of cell death in the perinatal mouse forebrain.The Journal of comparative neurology · 2017Article
- Targeting Adult Neurogenesis for Poststroke Therapy.Stem cells international · 2017Review
- Control of adult neurogenesis by programmed cell death in the mammalian brain.Molecular brain · 2016Review
- Elimination of aberrant DRG circuitries in Sema3A mutant mice leads to extensive neuronal deficits.PloS one · 2013Article
- Sustained Hox5 gene activity is required for respiratory motor neuron development.Nature neuroscience · 2012Article
- Motor neuron trophic factors: therapeutic use in ALS?Brain research reviews · 2011Review
- Changes in the Histone Acetylation Patterns during the Development of the Nervous System.Experimental neurobiology · 2011Article
- ZPK/DLK, a mitogen-activated protein kinase kinase kinase, is a critical mediator of programmed cell death of motoneurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011Article
- Article
- Characterization of sensory neurons in the dorsal root ganglia of Bax-deficient mice.Brain research · 2010Article
- Telomerase deficiency affects normal brain functions in mice.Neurochemical research · 2010Article
- Abnormal development of the neuromuscular junction in Nedd4-deficient mice.Developmental biology · 2009Article
- The maintenance of specific aspects of neuronal function and behavior is dependent on programmed cell death of adult-generated neurons in the dentate gyrus.The European journal of neuroscience · 2009Article
- Sex differences in NeuN- and androgen receptor-positive cells in the bed nucleus of the stria terminalis are due to Bax-dependent cell death.Neuroscience · 2009Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The removal of excess neurons by programmed cell death (PCD) is believed to be critical for the proper development and function of the nervous system. A major role of this neuronal loss is to attain quantitative matching of neurons with their targets and afferents. Because motoneurons (MNs) in Bax knock-out (Bax KO) mice fail to undergo PCD in the face of normal target muscle development, we asked whether the excess rescued neurons in Bax KO mice can develop normally. We observed many small atrophied MNs in postnatal Bax KO mice, and these failed to innervate limb muscle targets. When examined embryonically during the PCD period, however, these excess MNs had initiated target innervation. To examine whether a limitation in trophic factor availability is responsible for postnatal MN atrophy and loss of innervation, we applied glial cell line-derived neurotrophic factor (GDNF) to neonatal mice. GDNF injection for 7-14 d induced the regrowth and reinnervation of muscle targets by atrophic MNs in Bax KO mice and prevented the normal postnatal death of MNs in wild-type mice. These results indicate that, although initially all of the MNs, including those rescued by Bax deletion, are able to project to and innervate targets, because of limited target-derived signals required for maintaining innervation and growth, only a subpopulation can grow and retain target contacts postnatally. Although sensory neurons in the dorsal root ganglia are also rescued from PCD by Bax deletion, their subsequent development is less affected than that of MNs.
Indexed as
Identifiers
12917363PMC6740454W2124003564What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.