ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2001
Motoneuron survival is enhanced in the absence of neuromuscular junction formation in embryos.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 39 citations in OpenAlex.
- Acetylcholine receptors from human muscle as pharmacological targets for ALS therapy.Proceedings of the National Academy of Sciences of the United States of America · 2016Trial
- Riluzole blocks human muscle acetylcholine receptors.The Journal of physiology · 2012Article
- Essential roles of the acetylcholine receptor gamma-subunit in neuromuscular synaptic patterning.Development (Cambridge, England) · 2008Article
- Retrograde signaling onto Ret during motor nerve terminal maturation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2008Article
- Astrocyte and muscle-derived secreted factors differentially regulate motoneuron survival.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2007Article
- Neuromuscular development in the absence of programmed cell death: phenotypic alteration of motoneurons and muscle.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2006Article
- Aberrant morphology and residual transmitter release at the Munc13-deficient mouse neuromuscular synapse.Molecular and cellular biology · 2005Article
- Glycinergic and GABAergic synaptic activity differentially regulate motoneuron survival and skeletal muscle innervation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2005Article
- Neuromuscular development after the prevention of naturally occurring neuronal death by Bax deletion.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2003Article
- Differential effects of neurotrophins and schwann cell-derived signals on neuronal survival/growth and synaptogenesis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2003Article
- Aberrant patterning of neuromuscular synapses in choline acetyltransferase-deficient mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2003Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Approximately half of the motoneurons produced during development die before birth or shortly after birth. Although it is believed that survival depends on a restricted supply of a trophic sustenance produced by the synaptic target tissue (i.e., muscle), it is unclear whether synapse formation per se is involved in motoneuron survival. To address this issue, we counted cranial motoneurons in a set of mutant mice in which formation of neuromuscular junctions is dramatically impaired (i.e., null mutants for agrin, nerve-derived agrin, rapsyn, and MuSK). We demonstrate that in the absence of synaptogenesis, there is an 18-34% increase in motoneuron survival in the facial, trochlear, trigeminal motor, and hypoglossal nuclei; the highest survival occurred in the MuSK-deficient animals in which synapse formation is most severely compromised. There was no change in the size of the mutant motoneurons as compared with control animals, and the morphology of the mutant motoneurons appeared normal. We postulate that the increased axonal branching observed in these mutants leads to a facilitated "access" of the motoneurons to muscle-derived trophic factors at sites other than synapses or that inactivity increases the production of such factors. Finally, we examined motoneurons in double mutants of CNTFRalpha(-/-) (in which there is a partial loss of motoneurons) and MuSK(-/-) (in which there is an increased survival of motoneurons). The motoneuron numbers in the double mutants parallel those of the single MuSK-deficient mice, indicating that synapse disruption can even overcome the deleterious effect of CNTFRalpha ablation.
Indexed as
Identifiers
11312299PMC6762561W2161887020What 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.