ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1998
Long-term desensitization of nicotinic acetylcholine receptors is regulated via protein kinase A-mediated phosphorylation.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
What it found
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Who cites it
34 citing papers in PubMed, 70 citations in OpenAlex.
- Neurobiological Mechanisms of Nicotine Reward and Aversion.Pharmacological reviews · 2022Review
- Pharmacogenetics factors influencing smoking cessation success; the importance of nicotine metabolism.Expert opinion on drug metabolism & toxicology · 2021Review
- Pathways for nicotinic receptor desensitization.The Journal of general physiology · 2020Article
- Article
- The Structure, Function, and Physiology of the Fetal and Adult Acetylcholine Receptor in Muscle.Frontiers in molecular neuroscience · 2020Review
- Article
- Rapsyn facilitates recovery from desensitization in fetal and adult acetylcholine receptors expressed in a muscle cell line.The Journal of physiology · 2019Article
- CHRNA4 and ANKK1 Polymorphisms Influence Smoking-Induced Nicotinic Acetylcholine Receptor Upregulation.Nicotine & tobacco research : official journal of the Society for Research on Nicotine and Tobacco · 2016Article
- Nicotinic modulation of hippocampal cell signaling and associated effects on learning and memory.Physiology & behavior · 2016Review
- Nonequivalent release sites govern synaptic depression.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Looking below the surface of nicotinic acetylcholine receptors.Trends in pharmacological sciences · 2015Review
- 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
- Zebrafish model for congenital myasthenic syndrome reveals mechanisms causal to developmental recovery.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Acetylcholine receptor gating in a zebrafish model for slow-channel syndrome.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- Increased nicotinic receptor desensitization in hypoglossal motor neurons following chronic developmental nicotine exposure.Journal of neurophysiology · 2012Article
- An acetylcholine receptor lacking both γ and ε subunits mediates transmission in zebrafish slow muscle synapses.The Journal of general physiology · 2011Article
- Adenosine A2A receptor induces protein kinase A-dependent functional modulation of human (alpha)3(beta)4 nicotinic receptor.The Journal of physiology · 2011Article
- 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
- Changes in cationic selectivity of the nicotinic channel at the rat ganglionic synapse: a role for chloride ions?PloS one · 2011Article
- Cross-regulation between colocalized nicotinic acetylcholine and 5-HT3 serotonin receptors on presynaptic nerve terminals.Acta pharmacologica Sinica · 2009Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
During prolonged application of transmitter, ligand-gated ion channels enter a nonconducting desensitized state. Studies on Torpedo electroplax nicotinic acetylcholine (ACh) receptors have shown that entry into the desensitized state is accelerated by protein kinase A-dependent (PKA) receptor phosphorylation. To examine the effects of phosphorylation on desensitization of muscle-type ACh receptors, we expressed the frog embryonic receptor type in Xenopus oocytes. Treatment of embryonic muscle ACh receptors with 8-Br cAMP had no measurable effect on the rate of entry into a desensitized state, but it greatly accelerated the recovery from desensitization. Three complementary approaches to reduce the levels of receptor phosphorylation provided additional evidence for a role of PKA-dependent phosphorylation in rescuing receptors from long-term desensitization. Inactivation of the endogenous PKA activity by coexpression of an inhibitor protein, treatment of receptors with phosphatase, and removal of phosphorylation sites by site-specific subunit mutation all resulted in slowed recovery. Our findings point to the existence of two distinct desensitized states: one requiring several seconds for full recovery and a second state from which recovery requires minutes. Receptors lacking PKA phosphorylation sites exhibit a pronounced increase in the slowly recovering component of desensitization, suggesting that receptor phosphorylation speeds overall recovery by reducing the entry into a deep desensitized state. This newly described effect of phosphorylation on ACh receptor function may serve as an important modulator of postsynaptic receptor sensitivity.
Indexed as
Identifiers
9801362PMC6792874W1488165876What OpenQuestion holds
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.