ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2012
Native α6β4* nicotinic receptors control exocytosis in human chromaffin cells of the adrenal gland.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 28 citations in OpenAlex.
- Nicotinic Receptors in Human Chromaffin Cells: Characterization, Functional and Physical Interactions between Subtypes and Regulation.International journal of molecular sciences · 2024Review
- A Novel α4/7-Conotoxin QuIA Selectively Inhibits α3β2 and α6/α3β4 Nicotinic Acetylcholine Receptor Subtypes with High Efficacy.Marine drugs · 2022Article
- Cross Talk between α7 and α3β4 Nicotinic Receptors Prevents Their Desensitization in Human Chromaffin Cells.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- A Variant in the Nicotinic Acetylcholine Receptor Alpha 3 Subunit Gene Is Associated With Hypertension Risks in Hypogonadic Patients.Frontiers in genetics · 2020Article
- α-Conotoxin VnIB from Conus ventricosus is a potent and selective antagonist of α6β4* nicotinic acetylcholine receptors.Neuropharmacology · 2019Article
- Insights Into Nicotinic Receptor Signaling in Nicotine Addiction: Implications for Prevention and Treatment.Current neuropharmacology · 2018Review
- Human nicotinic receptors in chromaffin cells: characterization and pharmacology.Pflugers Archiv : European journal of physiology · 2018Review
- Nerve Stimulation: Immunomodulation and Control of Inflammation.Trends in molecular medicine · 2017Review
- TC299423, a Novel Agonist for Nicotinic Acetylcholine Receptors.Frontiers in pharmacology · 2017Article
- α-Conotoxins Identify the α3β4* Subtype as the Predominant Nicotinic Acetylcholine Receptor Expressed in Human Adrenal Chromaffin Cells.Molecular pharmacology · 2015Article
- Review
- Roles for N-terminal extracellular domains of nicotinic acetylcholine receptor (nAChR) β3 subunits in enhanced functional expression of mouse α6β2β3- and α6β4β3-nAChRs.The Journal of biological chemistry · 2014Article
- Diverse strategies targeting α7 homomeric and α6β2* heteromeric nicotinic acetylcholine receptors for smoking cessation.Annals of the New York Academy of Sciences · 2014Review
- Article
- Article
- Elucidation of molecular impediments in the α6 subunit for in vitro expression of functional α6β4* nicotinic acetylcholine receptors.The Journal of biological chemistry · 2013Article
- α-Conotoxin PeIA[S9H,V10A,E14N] potently and selectively blocks α6β2β3 versus α6β4 nicotinic acetylcholine receptors.Molecular pharmacology · 2012Article
- Functional chromaffin cell plasticity in response to stress: focus on nicotinic, gap junction, and voltage-gated Ca2+ channels.Journal of molecular neuroscience : MN · 2012Review
- Nicotinic acetylcholine receptors in dorsal root ganglion neurons include the α6β4* subtype.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2012Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
In the present study, we have electrophysiologically characterized native nicotinic acetylcholine receptors (nAChRs) in human chromaffin cells of the adrenal gland as well as their contribution to the exocytotic process. α-Conotoxin AuIB blocked by 14 ± 1% the acetylcholine (ACh)-induced nicotinic current. α-Conotoxin MII (α-Ctx MII) exhibited an almost full blockade of the nicotinic current at nanomolar concentrations (IC(50)=21.6 nM). The α6*-preferring α-Ctx MII mutant analogs, α-Ctx MII[H9A,L15A] and α-Ctx MII[S4A,E11A,L15A], blocked nAChR currents with an IC(50) of 217.8 and 33 nM, respectively. These data reveal that nAChRs in these cells include the α6* subtype. The washout of the blockade exerted by α-conotoxin BuIA (α-Ctx BuIA; 1 μM) on ACh-evoked currents was slight and slow, arguing in favor of the presence of a β4 subunit in the nAChR composition. Exocytosis was almost fully blocked by 1 μM α-Ctx MII, its mutant analogs, or α-Ctx BuIA. Finally, the fluorescent analog Alexa Fluor 546-BuIA showed distinct staining in these cells. Our results reveal that α6β4* nAChRs are expressed and contribute to exocytosis in human chromaffin cells of the adrenal gland, the main source of adrenaline under stressful situations.
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