ArticleActa pharmacologica Sinica2009
Kinetics of desensitization and recovery from desensitization for human alpha4beta2-nicotinic acetylcholine receptors stably expressed in SH-EP1 cells.
Article in Acta pharmacologica Sinica, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed.
- Evaluation of Pyrene Induced Cardiotoxicity Using Dual-Cardiotoxicity Evaluation Method.International journal of stem cells · 2026Article
- Bidirectional Modulation of Beam Traversal Performance by Acetylcholine in the Cerebellar Nuclei.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Article
- Structural insights into the progressive recovery of α7 nicotinic acetylcholine receptor from nicotine-induced desensitization.Science advances · 2025Article
- Minding the gap between artificial and biological computing paradigms for biologically loyal AI.Frontiers in systems neuroscience · 2025Article
- Cocaine Directly Inhibits α6-Containing Nicotinic Acetylcholine Receptors in Human SH-EP1 Cells and Mouse VTA DA Neurons.Frontiers in pharmacology · 2019Article
- Pauses in cholinergic interneuron firing exert an inhibitory control on striatal output in vivo.eLife · 2018Article
- Nicotinic and opioid receptor regulation of striatal dopamine D2-receptor mediated transmission.Scientific reports · 2016Article
- Differential modulation of GABAA and NMDA receptors by α7-nicotinic receptor desensitization in cultured rat hippocampal neurons.Acta pharmacologica Sinica · 2016Article
- A Novel α2/α4 Subtype-selective Positive Allosteric Modulator of Nicotinic Acetylcholine Receptors Acting from the C-tail of an α Subunit.The Journal of biological chemistry · 2015Article
- Going up in smoke? A review of nAChRs-based treatment strategies for improving cognition in schizophrenia.Current pharmaceutical design · 2014Review
- Augmentation of cognitive function by NS9283, a stoichiometry-dependent positive allosteric modulator of α2- and α4-containing nicotinic acetylcholine receptors.British journal of pharmacology · 2012Article
- Modulation of recombinant, α2*, α3* or α4*-nicotinic acetylcholine receptor (nAChR) function by nAChR β3 subunits.Journal of neurochemistry · 2012Article
- VUF10166, a novel compound with differing activities at 5-HT₃A and 5-HT₃AB receptors.The Journal of pharmacology and experimental therapeutics · 2012Article
- Effects of nicotine on depressive-like behavior and hippocampal volume of female WKY rats.Progress in neuro-psychopharmacology & biological psychiatry · 2010Article
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4 authors.
Funding
Abstract
aimStudies were conducted to define the kinetics of the onset of and recovery from desensitization for human alpha4beta2-nicotinic acetylcholine receptors (nAChR) heterologously expressed in the SH-EP1 human epithelial cell line.
methodsWhole-cell patch clamp recordings were performed to evaluate alpha4beta2-nAChR currents.
resultsApplication of 0.1 micromol/L nicotine or 1 mmol/L acetylcholine (ACh) for 1 s or longer induced two phases, with time constants of approximately 70 and approximately 700 ms, for the onset of alpha4beta2-nAChR desensitization. For a given duration of agonist exposure, recovery from desensitization induced by nicotine was slower than recovery from ACh-induced desensitization. Comparisons with published reports indicate that time constants for the recovery of alpha4beta2-nAChRs from desensitization are smaller than those for the recovery of human muscle-type nAChRs(1) from desensitization produced by the same concentrations and durations of exposure to an agonist. Moreover, the extent of human alpha4beta2-nAChR desensitization and rate of recovery are the same, regardless of whether they are measured using whole-cell recording or based on published findings(2) using isotopic ion flux assays; this equality demonstrates the equivalent legitimacy of these techniques in the evaluation of nAChR desensitization. Perhaps most significantly, recovery from desensitization also was best fit to a biphasic process. Regardless of whether it was fit to single or double exponentials, however, half-times for recovery from desensitization grew progressively longer with an increased duration of agonist exposure during the desensitizing pulse.
conclusionThese findings indicate the existence of alpha4beta2-nAChRs in many distinctive states of desensitization, as well as the induction of progressively deeper states of desensitization with the increased duration of agonist exposure.
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