ArticleProceedings of the National Academy of Sciences of the United States of America2003
Altered properties of quantal neurotransmitter release at endplates of mice lacking P/Q-type Ca2+ channels.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 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
55 citing papers in PubMed, 127 citations in OpenAlex.
- Cholesterol-Lowering Treatment Suppresses Neuromuscular Transmission Via Presynaptic Mechanism at the Mouse Diaphragm Muscle.Neurochemical research · 2025Article
- 25-Hydroxycholesterol modulates synaptic vesicle endocytosis at the mouse neuromuscular junction.Pflugers Archiv : European journal of physiology · 2025Article
- The Mechanism of α2 adrenoreceptor-dependent Modulation of Neurotransmitter Release at the Neuromuscular Junctions.Neurochemical research · 2024Article
- Simulations of active zone structure and function at mammalian NMJs predict that loss of calcium channels alone is not sufficient to replicate LEMS effects.Journal of neurophysiology · 2023Article
- Neuromuscular recovery from botulism involves multiple forms of compensatory plasticity.Frontiers in cellular neuroscience · 2023Article
- Roles and Sources of Calcium in Synaptic Exocytosis.Advances in neurobiology · 2023Article
- Sympathomimetics regulate neuromuscular junction transmission through TRPV1, P/Q- and N-type CaMolecular and cellular neurosciences · 2019Article
- Transmitter release site organization can predict synaptic function at the neuromuscular junction.Journal of neurophysiology · 2018Article
- Limitations and Challenges in Modeling Diseases Involving Spinal Motor Neuron DegenerationFrontiers in cellular neuroscience · 2018Article
- Lambert-Eaton myasthenic syndrome: mouse passive-transfer model illuminates disease pathology and facilitates testing therapeutic leads.Annals of the New York Academy of Sciences · 2018Review
- Muscle Contraction Regulates BDNF/TrkB Signaling to Modulate Synaptic Function through Presynaptic cPKCα and cPKCβI.Frontiers in molecular neuroscience · 2017Article
- The role of laminins in the organization and function of neuromuscular junctions.Matrix biology : journal of the International Society for Matrix Biology · 2017Review
- Redistribution of Cav2.1 channels and calcium ions in nerve terminals following end-to-side neurorrhaphy: ionic imaging analysis by TOF-SIMS.Histochemistry and cell biology · 2016Article
- Tick holocyclotoxins trigger host paralysis by presynaptic inhibition.Scientific reports · 2016Article
- Defects in Neuromuscular Transmission May Underlie Motor Dysfunction in Spinal and Bulbar Muscular Atrophy.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- Altered short-term synaptic plasticity and reduced muscle strength in mice with impaired regulation of presynaptic CaV2.1 Ca2+ channels.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- The Role of Calcium Channels in Epilepsy.Cold Spring Harbor perspectives in medicine · 2016Review
- Synaptic Vesicle Proteins and Active Zone Plasticity.Frontiers in synaptic neuroscience · 2016Article
- The Physiology, Pathology, and Pharmacology of Voltage-Gated Calcium Channels and Their Future Therapeutic Potential.Pharmacological reviews · 2015Review
- Synaptic Pathophysiology and Treatment of Lambert-Eaton Myasthenic Syndrome.Molecular neurobiology · 2015Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Transmission at the mouse neuromuscular junction normally relies on P/Q-type channels, but became jointly dependent on both N- and R-type Ca(2+) channels when the PQ-type channel alpha(1A) subunit was deleted. R-type channels lay close to Ca(2+) sensors for exocytosis and I(K(Ca)) channel activation, like the P/Q-type channels they replaced. In contrast, N-type channels were less well localized, but abundant enough to influence secretion strongly, particularly when action potentials were prolonged. Our data suggested that active zone structures may select among multiple Ca(2+) channels in the hierarchy P/Q >R >N. The alpha(1A)-/- neuromuscular junction displayed several other differences from wild-type: lowered quantal content but greater ability to withstand reductions in the Ca(2+)/Mg(2+) ratio, and little or no paired-pulse facilitation, the latter findings possibly reflecting compensatory mechanisms at individual release sites. Changes in presynaptic function were also associated with a significant reduction in the size of postsynaptic acetylcholine receptor clusters.
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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.