ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2000
Reduction of neuromuscular activity is required for the rescue of motoneurons from naturally occurring cell death by nicotinic-blocking agents.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
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The trial behind it
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Who cites it
24 citing papers in PubMed, 54 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
- Structure and Function of the Mammalian Neuromuscular Junction.Comprehensive Physiology · 2022Article
- Blocking skeletal muscle DHPRs/Ryr1 prevents neuromuscular synapse loss in mutant mice deficient in type III Neuregulin 1 (CRD-Nrg1).PLoS genetics · 2019Article
- Differences in lumbar motor neuron pruning in an animal model of early onset spasticity.Journal of neurophysiology · 2018Article
- Thioredoxin-2 Modulates Neuronal Programmed Cell Death in the Embryonic Chick Spinal Cord in Basal and Target-Deprived Conditions.PloS one · 2015Article
- Differential effects of RET and TRKB on axonal branching and survival of parasympathetic neurons.Developmental neurobiology · 2013Article
- Genetic deficiency of GABA differentially regulates respiratory and non-respiratory motor neuron development.PloS one · 2013Article
- Riluzole blocks human muscle acetylcholine receptors.The Journal of physiology · 2012Article
- Glial cell line-derived neurotrophic factor protein content in rat skeletal muscle is altered by increased physical activity in vivo and in vitro.Neuroscience · 2011Article
- Novel mouse model reveals distinct activity-dependent and -independent contributions to synapse development.PloS one · 2011Article
- Article
- Prostate stem cell antigen is an endogenous lynx1-like prototoxin that antagonizes alpha7-containing nicotinic receptors and prevents programmed cell death of parasympathetic neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2009Article
- The vesicular acetylcholine transporter is required for neuromuscular development and function.Molecular and cellular biology · 2009Article
- Inhibition of electrical activity by retroviral infection with Kir2.1 transgenes disrupts electrical differentiation of motoneurons.PloS one · 2008Article
- Essential roles of the acetylcholine receptor gamma-subunit in neuromuscular synaptic patterning.Development (Cambridge, England) · 2008Article
- Astrocyte and muscle-derived secreted factors differentially regulate motoneuron survival.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2007Article
- Phosphorylation of c-Jun in avian and mammalian motoneurons in vivo during programmed cell death: an early reversible event in the apoptotic cascade.The Journal of neuroscience : the official journal of the Society for Neuroscience · 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
- 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
Spinal motoneurons (MNs) in the chick embryo undergo programmed cell death coincident with the establishment of nerve-muscle connections and the onset of synaptic transmission at the neuromuscular junction. Chronic treatment of embryos during this period with nicotinic acetylcholine receptor (nAChR)-blocking agents [e.g., curare or alpha-bungarotoxin (alpha-BTX)] prevents the death of MNs. Although this rescue effect has been attributed previously to a peripheral site of action of the nAChR-blocking agents at the neuromuscular junction (NMJ), because nAChRs are expressed in both muscle and spinal cord, it has been suggested that the rescue effect may, in fact, be mediated by a direct central action of nAChR antagonists. By using a variety of different nAChR-blocking agents that target specific muscle or neuronal nAChR subunits, we find that only those agents that act on muscle-type receptors block neuromuscular activity and rescue MNs. However, paralytic, muscular dysgenic mutant chick embryos also exhibit significant increases in MN survival that can be further enhanced by treatment with curare or alpha-BTX, suggesting that muscle paralysis may not be the sole factor involved in MN survival. Taken together, the data presented here support the argument that, in vivo, nAChR antagonists promote the survival of spinal MNs primarily by acting peripherally at the NMJ to inhibit synaptic transmission and reduce or block muscle activity. Although a central action of these agents involving direct perturbations of MN activity may also play a contributory role, further studies are needed to determine more precisely the relative roles of central versus peripheral sites of action in MN rescue.
Indexed as
Identifiers
10934261PMC6772570W2154603822What 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.