ArticleMolecular and cellular biology2009
The vesicular acetylcholine transporter is required for neuromuscular development and function.
Article in Molecular and cellular biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.
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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
66 citing papers in PubMed, 126 citations in OpenAlex.
- Acetylcholine in Brain-Body Communication: Biological Mechanisms and Physiological Roles.International journal of molecular sciences · 2026Review
- Article
- Exogenous Administration of Delta-9-Tetrahydrocannabinol Affects Adult Hippocampal Neurotransmission in Female Wistar Rats.International journal of molecular sciences · 2025Article
- Binding mechanism and antagonism of the vesicular acetylcholine transporter VAChT.Nature structural & molecular biology · 2025Article
- Proenkephalin 119-159 in Heart Failure: From Pathophysiology to Clinical Implications.Journal of clinical medicine · 2025Review
- Multimodal gradients of basal forebrain connectivity across the neocortex.Nature communications · 2024Article
- Structural insights into VAChT neurotransmitter recognition and inhibition.Cell research · 2024Article
- Presynaptic Congenital Myasthenic Syndromes: Understanding Clinical Phenotypes through In vivo Models.Journal of neuromuscular diseases · 2023Review
- Human fetal membrane-mesenchymal stromal cells generate functional spinal motor neuronsiScience · 2022Article
- The Effect of α7nAChR Signaling on T Cells and Macrophages and Their Clinical Implication in the Treatment of Rheumatic Diseases.Neurochemical research · 2022Review
- Human mesenchymal amniotic fluid stem cells reveal an unexpected neuronal potential differentiating into functional spinal motor neurons.Frontiers in cell and developmental biology · 2022Article
- Article
- Phenotypical and Myopathological Consequences of Compound Heterozygous Missense and Nonsense Variants inCells · 2021Article
- Newly-Discovered Neural Features Expand the Pathobiological Knowledge of Blastic Plasmacytoid Dendritic Cell Neoplasm.Cancers · 2021Article
- Long-term endogenous acetylcholine deficiency potentiates pulmonary inflammation in a murine model of elastase-induced emphysema.Scientific reports · 2021Article
- Lung Edema and Mortality Induced by Intestinal Ischemia and Reperfusion Is Regulated by VAChT Levels in Female Mice.Inflammation · 2021Article
- Acute Lung Injury in Cholinergic-Deficient Mice Supports Anti-Inflammatory Role of α7 Nicotinic Acetylcholine Receptor.International journal of molecular sciences · 2021Article
- Functional and Biochemical Consequences of Disease Variants in Neurotransmitter Transporters: A Special Emphasis on Folding and Trafficking Deficits.Pharmacology & therapeutics · 2021Review
- Changes in the Gene Expression Profiles of the Inferior Colliculus Following Unilateral Cochlear Ablation in Adult Rats.Biochemical genetics · 2021Article
- Variants ofBMJ case reports · 2021Article
6 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
21 authors at 5 institutions in 3 countries.
Funding
Abstract
The vesicular acetylcholine (ACh) transporter (VAChT) mediates ACh storage by synaptic vesicles. However, the VAChT-independent release of ACh is believed to be important during development. Here we generated VAChT knockout mice and tested the physiological relevance of the VAChT-independent release of ACh. Homozygous VAChT knockout mice died shortly after birth, indicating that VAChT-mediated storage of ACh is essential for life. Indeed, synaptosomes obtained from brains of homozygous knockouts were incapable of releasing ACh in response to depolarization. Surprisingly, electrophysiological recordings at the skeletal-neuromuscular junction show that VAChT knockout mice present spontaneous miniature end-plate potentials with reduced amplitude and frequency, which are likely the result of a passive transport of ACh into synaptic vesicles. Interestingly, VAChT knockouts exhibit substantial increases in amounts of choline acetyltransferase, high-affinity choline transporter, and ACh. However, the development of the neuromuscular junction in these mice is severely affected. Mutant VAChT mice show increases in motoneuron and nerve terminal numbers. End plates are large, nerves exhibit abnormal sprouting, and muscle is necrotic. The abnormalities are similar to those of mice that cannot synthesize ACh due to a lack of choline acetyltransferase. Our results indicate that VAChT is essential to the normal development of motor neurons and the release of ACh.
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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.