ArticleBiophysical journal1993
A molecular scheme for the reaction between acetylcholine and nicotinic channels.
Article in Biophysical journal, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed.
- Pathways for nicotinic receptor desensitization.The Journal of general physiology · 2020Article
- The dual-gate model for pentameric ligand-gated ion channels activation and desensitization.The Journal of physiology · 2018Review
- Activation of endplate nicotinic acetylcholine receptors by agonists.Biochemical pharmacology · 2015Review
- Agonists binding nicotinic receptors elicit specific channel-opening patterns at αγ and αδ sites.The Journal of physiology · 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
- The structural mechanism of the Cys-loop receptor desensitization.Molecular neurobiology · 2013Review
- Desensitization of neurotransmitter-gated ion channels during high-frequency stimulation: a comparative study of Cys-loop, AMPA and purinergic receptors.The Journal of physiology · 2011Article
- Bridging the gap between structural models of nicotinic receptor superfamily ion channels and their corresponding functional states.Journal of molecular biology · 2010Article
- Modeling nicotinic neuromodulation from global functional and network levels to nAChR based mechanisms.Acta pharmacologica Sinica · 2009Review
- Desensitization contributes to the synaptic response of gain-of-function mutants of the muscle nicotinic receptor.The Journal of general physiology · 2006Article
- Block of muscle nicotinic receptors by choline suggests that the activation and desensitization gates act as distinct molecular entities.The Journal of general physiology · 2006Article
- Desensitization of alpha7 nicotinic receptors potentiated the inhibitory effect on M-current induced by stimulation of muscarinic receptors in rat superior cervical ganglion neurons.Journal of neural transmission (Vienna, Austria : 1996) · 2005Article
- Activation of heteroliganded mouse muscle nicotinic receptors.The Journal of physiology · 2005Article
- Short openings in high resolution single channel recordings of mouse nicotinic receptors.The Journal of physiology · 2005Article
- Properties of the human muscle nicotinic receptor, and of the slow-channel myasthenic syndrome mutant epsilonL221F, inferred from maximum likelihood fits.The Journal of physiology · 2003Article
- Desensitization of diliganded mouse muscle nicotinic acetylcholine receptor channels.The Journal of physiology · 2002Article
- Acetylcholine receptor channel structure in the resting, open, and desensitized states probed with the substituted-cysteine-accessibility method.Proceedings of the National Academy of Sciences of the United States of America · 2001Article
- Serum choline activates mutant acetylcholine receptors that cause slow channel congenital myasthenic syndromes.Proceedings of the National Academy of Sciences of the United States of America · 1999Article
- Two mutations linked to nocturnal frontal lobe epilepsy cause use-dependent potentiation of the nicotinic ACh response.The Journal of physiology · 1998Article
- Defining affinity with the GABAA receptor.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1998Article
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In outside-out patches of mouse-muscle membrane, embryonic-like channels were activated by pulses of acetylcholine (ACh). On increasing the ACh concentration, the rate of desensitization, 1/tau d, increased linearly with the peak open probability, indicating desensitization from the open state. Desensitization had only one time constant tau d at each ACh concentration. Recovery from desensitization was only approximately 10 times slower than desensitization, whereas the probability of steady-state channel opening, declined to < 0.01 with > 10(-6) M ACh. The peak probability of opening in > 10(-4) M ACh pulse was close to 1. A linear reaction scheme was not compatible with these results. The scheme had to be expanded resulting in a circular scheme with two additional ACh binding steps to desensitized channel states. The approximate rate constants of all reaction steps in the circular scheme could be determined using computer simulations. The model predicted that clusters of channel opening had the average duration tau d at the respective ACh concentration. In cell-attached patches on intact muscle fibers, similar average cluster durations were observed at the respective ACh concentration. This indicates that tau d in the intact muscle fibers has similar values as in outside-out patches.
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