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Stable expression in HEK‐293 cells of the rat α3/β4 subtype of neuronal nicotinic acetylcholine receptor
Author(s) -
Stetzer Eva,
Ebbinghaus Ullrich,
Storch Alexander,
Poteur Livia,
Schrattenholz Andre,
Kramer Gert,
Methfessel Christoph,
Maelicke Alfred
Publication year - 1996
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(96)01115-5
Subject(s) - nicotinic antagonist , nicotinic agonist , muscarinic acetylcholine receptor , acetylcholine , hek 293 cells , acetylcholine receptor , chemistry , nicotinic acetylcholine receptor , cytisine , alpha 4 beta 2 nicotinic receptor , ganglion type nicotinic receptor , methyllycaconitine , patch clamp , pharmacology , nicotine , mecamylamine , ion channel , muscarinic acetylcholine receptor m3 , biophysics , receptor , biology , neuroscience , biochemistry
The α3/β4 subtype of neuronal nicotinic acetylcholine receptor (nAChR) was stably expressed in human embryonic kidney (HEK) 293 cells that co‐expressed a voltage‐gated Ca 2+ channel. α3/β4‐nAChR‐expressing clones were identified using the fura‐2 Ca 2+ imaging technique, and were further characterised by single‐cell and whole‐cell patch‐clamp studies. Acetylcholine (ACh) induced fast activating currents which showed desensitisation and inward rectification. The conductance of the ACh‐activated channel was 29 pS. The order of potency of the nicotinic agonists tested was . The EC 50 value for ACh was 145 μM; the Hill coefficient was close to 2. The currents elicited by ACh were effectively blocked by nicotinic antagonists, but not by the muscarinic antagonist atropine. These properties are comparable to the pharmacological and physiological profile of ganglionic nicotinic receptors and type III currents of cultured hippocampal neurons.