ArticleBritish journal of pharmacology2015
PKCε phosphorylates α4β2 nicotinic ACh receptors and promotes recovery from desensitization.
Article in British journal of pharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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13 citing papers in PubMed, 17 citations in OpenAlex.
- Structural insights into the progressive recovery of α7 nicotinic acetylcholine receptor from nicotine-induced desensitization.Science advances · 2025Article
- Tyrosine phosphorylation differentially fine-tunes ionotropic and metabotropic responses of human α7 nicotinic acetylcholine receptor.Cellular and molecular life sciences : CMLS · 2021Article
- Compensatory mechanisms in resistant Anopheles gambiae AcerKis and KdrKis neurons modulate insecticide-based mosquito control.Communications biology · 2021Article
- Addiction-related neuroadaptations following chronic nicotine exposure.Journal of neurochemistry · 2021Review
- Bidirectional sex-dependent regulation of α6 and β3 nicotinic acetylcholine receptors by protein kinase Cε.Addiction biology · 2021Article
- Evaluation of the Phosphoproteome of Mouse Alpha 4/Beta 2-Containing Nicotinic Acetylcholine Receptors In Vitro and In Vivo.Proteomes · 2018Article
- Reviewing the Diverse Effects of Protein Phosphorylation in Neural Signaling Transduction.Journal of undergraduate neuroscience education : JUNE : a publication of FUN, Faculty for Undergraduate Neuroscience · 2018Article
- ACh-induced hyperpolarization and decreased resistance in mammalian type II vestibular hair cells.Journal of neurophysiology · 2018Article
- P/Q-type voltage-gated calcium channels mediate the ethanol and CRF sensitivity of central amygdala GABAergic synapses.Neuropharmacology · 2017Article
- Odorant Receptor Sensitivity Modulation inThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- Alcohol Dependence Disrupts Amygdalar L-Type Voltage-Gated Calcium Channel Mechanisms.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- Weight of evidence evaluation of a network of adverse outcome pathways linking activation of the nicotinic acetylcholine receptor in honey bees to colony death.The Science of the total environment · 2017Review
- Probing the Allosteric Role of the α5 Subunit of α3β4α5 Nicotinic Acetylcholine Receptors by Functionally Selective Modulators and Ligands.ACS chemical biology · 2017Article
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
Abstract
background and purposeNicotinic (ACh) receptor recovery from desensitization is modulated by PKC, but the PKC isozymes and the phosphorylation sites involved have not been identified. We investigated whether PKCε phosphorylation of α4β2 nAChRs regulates receptor recovery from desensitization. EXPERIMENTAL APPROACH: Receptor recovery from desensitization was investigated by electrophysiological characterization of human α4β2 nAChRs. Phosphorylation of the α4 nAChR subunit was assessed by immunoblotting of mouse synaptosomes. Hypothermia induced by sazetidine-A and nicotine was measured in Prkce(-/-) and wild-type mice. KEY
resultsInhibiting PKCε impaired the magnitude of α4β2 nAChR recovery from desensitization. We identified five putative PKCε phosphorylation sites in the large intracellular loop of the α4 subunit, and mutating four sites to alanines also impaired recovery from desensitization. α4 nAChR subunit phosphorylation was reduced in synaptosomes from Prkce(-/-) mice. Sazetidine-A-induced hypothermia, which is mediated by α4β2 nAChR desensitization, was more severe and prolonged in Prkce(-/-) than in wild-type mice. CONCLUSIONS AND IMPLICATIONS: PKCε phosphorylates the α4 nAChR subunit and regulates recovery from receptor desensitization. This study illustrates the importance of phosphorylation in regulating α4β2 receptor function, and suggests that reducing phosphorylation prolongs receptor desensitization and decreases the number of receptors available for activation.
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