ReviewThe Journal of physiology2012
Reactive oxygen species inactivate neuronal nicotinic acetylcholine receptors through a highly conserved cysteine near the intracellular mouth of the channel: implications for diseases that involve oxidative stress.
Review in The Journal of physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 41 citations in OpenAlex.
- Mechanistic insights into taxane-induced psychiatric adverse events: a global pharmacovigilance and experimental investigation.Molecular psychiatry · 2026Article
- Oxidative stress and atrial fibrillation.Journal of molecular and cellular cardiology · 2024Review
- Patient-specific variants of NFU1/NFU-1 disrupt cholinergic signaling in a model of multiple mitochondrial dysfunctions syndrome 1.Disease models & mechanisms · 2023Article
- Cognitive dysfunction in diabetes: abnormal glucose metabolic regulation in the brain.Frontiers in endocrinology · 2023Review
- Opposite Regulation of Homer Signal at the NMJ Postsynaptic Micro Domain between Slow- and Fast-Twitch Muscles in an Experimentally Induced Autoimmune Myasthenia Gravis (EAMG) Mouse Model.International journal of molecular sciences · 2022Article
- Role of α7 Nicotinic Acetylcholine Receptors in Synaptic Transmission in Frog Neuromuscular Contacts.Bulletin of experimental biology and medicine · 2022Article
- Nicotine and vascular dysfunction.Acta physiologica (Oxford, England) · 2021Review
- Reduced Cell Excitability of Cardiac Postganglionic Parasympathetic Neurons Correlates With Myocardial Infarction-Induced Fatal Ventricular Arrhythmias in Type 2 Diabetes Mellitus.Frontiers in neuroscience · 2021Article
- Increased arrhythmia susceptibility in type 2 diabetic mice related to dysregulation of ventricular sympathetic innervation.American journal of physiology. Heart and circulatory physiology · 2019Article
- Nurr1, Pitx3, and α7 nAChRs mRNA Expression in Nigral Tissue of Rats with Pedunculopontine Neurotoxic Lesion.Medicina (Kaunas, Lithuania) · 2019Article
- MicroRNAs in Microglia: How do MicroRNAs Affect Activation, Inflammation, Polarization of Microglia and Mediate the Interaction Between Microglia and Glioma?Frontiers in molecular neuroscience · 2019Review
- Influence of Resveratrol on Oxidation Processes and Lipid Phase Characteristics in Damaged Somatic Nerves.BioMed research international · 2019Article
- Oxidative Modification and Its Implications for the Neurodegeneration of Parkinson's Disease.Molecular neurobiology · 2017Review
- Low serum albumin concentrations are associated with disease severity in patients with myasthenia gravis.Medicine · 2016Observational
- Serum uric acid levels in patients with myasthenia gravis are inversely correlated with disability.Neuroreport · 2016Article
- Distribution and biomarkers of carbon-14-labeled fullerene C60 ([(14) C(U)]C60 ) in female rats and mice for up to 30 days after intravenous exposure.Journal of applied toxicology : JAT · 2015Article
- Synapses on sympathetic neurons and parasympathetic neurons differ in their vulnerability to diabetes.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- The role of intracellular linkers in gating and desensitization of human pentameric ligand-gated ion channels.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- FOXO1 locus and acetylcholinesterase inhibitors in elderly patients with Alzheimer's disease.Clinical interventions in aging · 2014Observational
- Diabetes impairs synaptic plasticity in the superior cervical ganglion: possible role for BDNF and oxidative stress.Journal of molecular neuroscience : MN · 2013Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
An intriguing feature of several nicotinic acetylcholine receptors (nAChRs) on neurons is that their subunits contain a highly conserved cysteine residue located near the intracellular mouth of the receptor pore. The work summarized in this review indicates that α3β4-containing and α4β2-containing neuronal nAChRs, and possibly other subtypes, are inactivated by elevations in intracellular reactive oxygen species (ROS). This review discusses a model for the molecular mechanisms that underlie this inactivation. In addition, we explore the implications of this mechanism in the context of complications that arise from diabetes. We review the evidence that diabetes elevates cytosolic ROS in sympathetic neurons and inactivates postsynaptic α3β4-containing nAChRs shortly after the onset of diabetes, leading to a depression of synaptic transmission in sympathetic ganglia, an impairment of sympathetic reflexes. These effects of ROS on nAChR function are due to the highly conserved Cys residues in the receptors: replacing the cysteine residues in α3 allow ganglionic transmission and sympathetic reflexes to function normally in diabetes. This example from diabetes suggests that other diseases involving oxidative stress, such as Parkinson's disease, could lead to the inactivation of nAChRs on neurons and disrupt cholinergic nicotinic signalling.
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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.