ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2006
Prolongation of evoked and spontaneous synaptic currents at the neuromuscular junction after activity blockade is caused by the upregulation of fetal acetylcholine receptors.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2006. 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, 17 citations in OpenAlex.
- The Structure, Function, and Physiology of the Fetal and Adult Acetylcholine Receptor in Muscle.Frontiers in molecular neuroscience · 2020Review
- Altered active zones, vesicle pools, nerve terminal conductivity, and morphology during experimental MuSK myasthenia gravis.PloS one · 2014Article
- Immobilization with atrophy induces de novo expression of neuronal nicotinic α7 acetylcholine receptors in muscle contributing to neurotransmission.Anesthesiology · 2014Article
- Acetylcholinesterase deficiency contributes to neuromuscular junction dysfunction in type 1 diabetic neuropathy.American journal of physiology. Endocrinology and metabolism · 2012Article
- Temporal requirement for high SMN expression in SMA mice.Human molecular genetics · 2011Article
- Impaired activity-dependent plasticity of quantal amplitude at the neuromuscular junction of Rab3A deletion and Rab3A earlybird mutant mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011Article
- Activity-dependent regulation of the binomial parameters p and n at the mouse neuromuscular junction in vivo.Journal of neurophysiology · 2010Article
- Reduced survival of motor neuron (SMN) protein in motor neuronal progenitors functions cell autonomously to cause spinal muscular atrophy in model mice expressing the human centromeric (SMN2) gene.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010Article
- Distinct muscarinic acetylcholine receptor subtypes contribute to stability and growth, but not compensatory plasticity, of neuromuscular synapses.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2009Article
- Impaired synaptic vesicle release and immaturity of neuromuscular junctions in spinal muscular atrophy mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2009Article
- Single-neuron labeling with inducible Cre-mediated knockout in transgenic mice.Nature neuroscience · 2008Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
It has been shown previously in a number of systems that after an extended block of activity, synaptic strength is increased. We found that an extended block of synaptic activity at the mouse neuromuscular junction, using a tetrodotoxin cuff in vivo, increased synaptic strength by prolonging the evoked endplate current (EPC) decay. Prolongation of EPC decay was accompanied by only modest prolongation of spontaneous miniature EPC (MEPC) decay. Prolongation of EPC decay was reversed when quantal content was lowered by reducing extracellular calcium. These findings suggested that the cause of EPC prolongation was presynaptic in origin. However, when we acutely inhibited fetal-type acetylcholine receptors (AChRs) using a novel peptide toxin (alphaA-conotoxin OIVA[K15N]), prolongation of both EPC and MEPC decay were reversed. We also blocked synaptic activity in a mutant strain of mice in which persistent muscle activity prevents upregulation of fetal-type AChRs. In these mice, there was no prolongation of EPC decay. We conclude that upregulation of fetal-type AChRs after blocking synaptic activity causes modest prolongation of MEPC decay that is accompanied by much greater prolongation of EPC decay. This might occur if acetylcholine escapes from endplates and binds to extrajunctional fetal-type AChRs only during large, evoked EPCs. Our study is the first to demonstrate a functional role for upregulation of extrajunctional AChRs.
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