ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2005
Galantamine activates muscle-type nicotinic acetylcholine receptors without binding to the acetylcholine-binding site.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 46 citations in OpenAlex.
- Targeting amyloid-β in Alzheimer's disease: A critical analysis of clinical trials and their implications for drug development.Iranian journal of basic medical sciences · 2026Review
- Therapeutic Strategies Aimed at Improving Neuroplasticity in Alzheimer Disease.Pharmaceutics · 2023Review
- Multi-Target Drug Candidates for Multifactorial Alzheimer's Disease: AChE and NMDAR as Molecular Targets.Molecular neurobiology · 2021Review
- Galantamine is not a positive allosteric modulator of human α4β2 or α7 nicotinic acetylcholine receptors.British journal of pharmacology · 2018Article
- Nicotinic acetylcholine receptors at the single-channel level.British journal of pharmacology · 2018Review
- Multi-Target Directed Donepezil-Like Ligands for Alzheimer's Disease.Frontiers in neuroscience · 2016Review
- ASS234, As a New Multi-Target Directed Propargylamine for Alzheimer's Disease Therapy.Frontiers in neuroscience · 2016Article
- Auto-inhibition at a ligand-gated ion channel: a cross-talk between orthosteric and allosteric sites.British journal of pharmacology · 2015Article
- Physostigmine and galanthamine bind in the presence of agonist at the canonical and noncanonical subunit interfaces of a nicotinic acetylcholine receptor.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Energetic contributions to channel gating of residues in the muscle nicotinic receptor β1 subunit.PloS one · 2013Article
- Physiological characterization of human muscle acetylcholine receptors from ALS patients.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- Young and older good learners have higher levels of brain nicotinic receptor binding.Neurobiology of aging · 2010Article
- The positive allosteric modulator morantel binds at noncanonical subunit interfaces of neuronal nicotinic acetylcholine receptors.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2009Article
- Mammalian nicotinic acetylcholine receptors: from structure to function.Physiological reviews · 2009Review
- Activation and block of the adult muscle-type nicotinic receptor by physostigmine: single-channel studies.Molecular pharmacology · 2008Article
- Identification of binding sites in the nicotinic acetylcholine receptor for TDBzl-etomidate, a photoreactive positive allosteric effector.The Journal of biological chemistry · 2008Article
- Morantel allosterically enhances channel gating of neuronal nicotinic acetylcholine alpha 3 beta 2 receptors.Molecular pharmacology · 2008Article
- Structural answers and persistent questions about how nicotinic receptors work.Frontiers in bioscience : a journal and virtual library · 2008Review
- Alpha7 nicotinic acetylcholine receptor: a link between inflammation and neurodegeneration.Neuroscience and biobehavioral reviews · 2008Review
- The alpha7 nicotinic acetylcholine receptor as a pharmacological target for inflammation.British journal of pharmacology · 2007Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Galantamine (Reminyl; Janssen Pharmaceutica, Titusville, NJ) belongs to a class of acetylcholinesterase inhibitors approved for symptomatic treatment of Alzheimer's disease. The drug presumably acts by raising and prolonging the profile of acetylcholine (ACh) via an inhibitory effect on the esterase. However, there is also evidence demonstrating that galantamine can activate the nicotinic ACh receptor or modulate its activation by ACh. In this study, we have examined the ability of galantamine to directly activate the muscle-type nicotinic ACh receptor or to modulate receptor activation by selected nicotinic agonists. Studies of direct activation by galantamine demonstrated that this ligand is a low-efficacy agonist of the muscle-type ACh receptor. Point mutations in the M2-M3 linker (alphaS269I) and the M2 transmembrane domain (epsilonT264P) had similar effects on receptor activation by galantamine and nicotinic agonists, suggesting that the general features of receptor activation by galantamine are similar to that in the presence of ACh. Experiments performed in the simultaneous presence of galantamine and various nicotinic ligands showed that channel activation by the nicotinic ligands studied (ACh, carbachol, and choline) was not affected by the presence of galantamine at concentrations up to 100 microm. In addition, galantamine did not reduce the initial rate of binding for 125I-alpha-bungarotoxin. These results demonstrate that galantamine does not interfere with the occupation of the nicotinic agonist binding site by ACh, carbachol, or choline. We conclude that galantamine activates the muscle-type ACh receptor by interacting with a binding site that is distinct from the site for nicotinic agonists.
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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.