ArticleThe Journal of physiology2003
Amyloid beta(1-42) peptide alters the gating of human and mouse alpha-bungarotoxin-sensitive nicotinic receptors.
Article in The Journal of physiology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 94 citations in OpenAlex.
- Co-activation of Selective Nicotinic Acetylcholine Receptor Subtypes Is Required for Neuroprotection against Alzheimer's Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Neuronal and Glial α7 Nicotinic Acetylcholine Receptors: Role in Alzheimer's Disease Pathophysiology.Life (Basel, Switzerland) · 2025Review
- Control of Synaptic Levels of Nicotinic Acetylcholine Receptor by the Sequestering Subunit Dα5 and Secreted Scaffold Protein Hig.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Discoveries and future significance of research into amyloid-beta/α7-containing nicotinic acetylcholine receptor (nAChR) interactions.Pharmacological research · 2023Review
- Physiological Roles of Monomeric Amyloid-β and Implications for Alzheimer's Disease Therapeutics.Experimental neurobiology · 2022Review
- Tetrapeptide Ac-HAEE-NHInternational journal of molecular sciences · 2020Article
- Molecular Modulation of Human α7 Nicotinic Receptor by Amyloid-β Peptides.Frontiers in cellular neuroscience · 2019Article
- The keystone of Alzheimer pathogenesis might be sought in Aβ physiology.Neuroscience · 2015Review
- The protein oxidation repair enzyme methionine sulfoxide reductase a modulates Aβ aggregation and toxicity in vivo.Antioxidants & redox signaling · 2015Article
- Nicotinic ACh receptors in the hippocampal circuit; functional expression and role in synaptic plasticity.The Journal of physiology · 2014Review
- Cholinergic receptors: functional role of nicotinic ACh receptors in brain circuits and disease.Pflugers Archiv : European journal of physiology · 2013Review
- Amyloid-β peptide: Dr. Jekyll or Mr. Hyde?Journal of Alzheimer's disease : JAD · 2013Review
- A cholinergic trigger drives learning-induced plasticity at hippocampal synapses.Nature communications · 2013Article
- Article
- Functional α7β2 nicotinic acetylcholine receptors expressed in hippocampal interneurons exhibit high sensitivity to pathological level of amyloid β peptides.BMC neuroscience · 2012Article
- Glutamatergic synapse formation is promoted by α7-containing nicotinic acetylcholine receptors.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- Virtual screening against acetylcholine binding protein.Journal of biomolecular screening · 2012Article
- Allosteric modulator Desformylflustrabromine relieves the inhibition of α2β2 and α4β2 nicotinic acetylcholine receptors by β-amyloid(1-42) peptide.Journal of molecular neuroscience : MN · 2011Article
- Endogenous signaling through alpha7-containing nicotinic receptors promotes maturation and integration of adult-born neurons in the hippocampus.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010Article
- Alzheimer's disease amyloid beta-protein and synaptic function.Neuromolecular medicine · 2010Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The beta-amyloid(1-42) peptide (Abeta(1-42)), a major constituent of the Alzheimer's disease amyloid plaque, specifically binds to the neuronal alpha-bungarotoxin (alpha-BuTx)-sensitive alpha7 nicotinic acetylcholine receptor (alpha7 nAChR). Accordingly, Abeta1-42 interferes with the function of alpha7 nAChRs in chick and rodent neurons. To gain insights into the human disease, we studied the action of Abeta(1-42) on human alpha7 nAChRs expressed in Xenopus oocytes. In voltage-clamped oocytes expressing the wild-type receptor, Abeta(1-42) blocked ACh-evoked currents. The block was non-competitive, required over 100 s to develop and was partially reversible. In oocytes expressing the mutant L248T receptor, Abeta(1-42) activated methyllycaconitine-sensitive currents in a dose-dependent manner. Peptide-evoked unitary events, recorded in outside-out patches, showed single-channel conductances and open duration comparable to ACh-evoked events. Abeta(1-42) had no effect on the currents evoked by glutamate, GABA or glycine in oocytes expressing human or mouse receptors for these transmitters. Muscle nAChRs are also alpha-BuTx-sensitive and we therefore investigated whether they respond to Abeta(1-42). In human kidney BOSC 23 cells expressing the fetal or adult mouse muscle nAChRs, Abeta(1-42) blocked ACh-evoked whole-cell currents, accelerating their decay. Outside-out single-channel recordings showed that the block was due to a reduced channel open probability and enhanced block upon ACh application. We also report that the inverse peptide Abeta(42-1), but not Abeta(40-1), partially mimicked the effects of the physiological Abeta(1-42) peptide. Possible implications for degenerative neuronal and muscular diseases are discussed.
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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.