Native α6β4* nicotinic receptors control exocytosis in human chromaffin cells of the adrenal gland.
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Native α6β4* nicotinic receptors control exocytosis in human chromaffin cells of the adrenal gland. / Perez-Alvarez, Alberto; Hernández-Vivanco, Alicia; McIntosh, J Michael; Albillos, Almudena.
in: FASEB J, Jahrgang 26, Nr. 1, 1, 2012, S. 346-354.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung
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T1 - Native α6β4* nicotinic receptors control exocytosis in human chromaffin cells of the adrenal gland.
AU - Perez-Alvarez, Alberto
AU - Hernández-Vivanco, Alicia
AU - McIntosh, J Michael
AU - Albillos, Almudena
PY - 2012
Y1 - 2012
N2 - 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. ?-Conotoxin AuIB blocked by 14 ± 1% the acetylcholine (ACh)-induced nicotinic current. ?-Conotoxin MII (?-Ctx MII) exhibited an almost full blockade of the nicotinic current at nanomolar concentrations (IC(50)=21.6 nM). The ?6*-preferring ?-Ctx MII mutant analogs, ?-Ctx MII[H9A,L15A] and ?-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 ?6* subtype. The washout of the blockade exerted by ?-conotoxin BuIA (?-Ctx BuIA; 1 ?M) on ACh-evoked currents was slight and slow, arguing in favor of the presence of a ?4 subunit in the nAChR composition. Exocytosis was almost fully blocked by 1 ?M ?-Ctx MII, its mutant analogs, or ?-Ctx BuIA. Finally, the fluorescent analog Alexa Fluor 546-BuIA showed distinct staining in these cells. Our results reveal that ?6?4* nAChRs are expressed and contribute to exocytosis in human chromaffin cells of the adrenal gland, the main source of adrenaline under stressful situations.
AB - 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. ?-Conotoxin AuIB blocked by 14 ± 1% the acetylcholine (ACh)-induced nicotinic current. ?-Conotoxin MII (?-Ctx MII) exhibited an almost full blockade of the nicotinic current at nanomolar concentrations (IC(50)=21.6 nM). The ?6*-preferring ?-Ctx MII mutant analogs, ?-Ctx MII[H9A,L15A] and ?-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 ?6* subtype. The washout of the blockade exerted by ?-conotoxin BuIA (?-Ctx BuIA; 1 ?M) on ACh-evoked currents was slight and slow, arguing in favor of the presence of a ?4 subunit in the nAChR composition. Exocytosis was almost fully blocked by 1 ?M ?-Ctx MII, its mutant analogs, or ?-Ctx BuIA. Finally, the fluorescent analog Alexa Fluor 546-BuIA showed distinct staining in these cells. Our results reveal that ?6?4* nAChRs are expressed and contribute to exocytosis in human chromaffin cells of the adrenal gland, the main source of adrenaline under stressful situations.
KW - Humans
KW - Cells, Cultured
KW - Patch-Clamp Techniques
KW - Acetylcholine/pharmacology
KW - Adrenal Medulla/physiology
KW - Cholinergic Agonists/pharmacology
KW - Chromaffin Cells/drug effects/physiology
KW - Conotoxins/pharmacology
KW - Exocytosis/drug effects/physiology
KW - Fluorescent Dyes/pharmacology
KW - Nicotinic Antagonists/pharmacology
KW - Quinolinium Compounds/pharmacology
KW - Receptors, Nicotinic/physiology
KW - Humans
KW - Cells, Cultured
KW - Patch-Clamp Techniques
KW - Acetylcholine/pharmacology
KW - Adrenal Medulla/physiology
KW - Cholinergic Agonists/pharmacology
KW - Chromaffin Cells/drug effects/physiology
KW - Conotoxins/pharmacology
KW - Exocytosis/drug effects/physiology
KW - Fluorescent Dyes/pharmacology
KW - Nicotinic Antagonists/pharmacology
KW - Quinolinium Compounds/pharmacology
KW - Receptors, Nicotinic/physiology
M3 - SCORING: Journal article
VL - 26
SP - 346
EP - 354
JO - FASEB J
JF - FASEB J
SN - 0892-6638
IS - 1
M1 - 1
ER -
