Neuronal nicotinic acetylcholine receptor subunits α3 (PCA48E) and β4S (ZPC13) were expressed in human embryonic kidney (HEK)-293 cells by calcium phosphate transfection. In the presence of atropine, acetylcholine (ACh) induced fast activating currents which exhibited desensitization and inward rectification. The EC50 for ACh was 202 ± 32 μM with a Hill coefficient of 1.9 ± 0.4. The rank order of nicotinic agonist potency was 1,1-dimethyl-4-phenylpiperozinium (DMPP) > cytisine = nicotine ≊ ACh. The maximal response elicited by DMPP was substantially less than that elicited by other agonists, suggesting that DMPP is a partial agonist. ACh (500 μM) responses were very effectively blocked by equimolar concentrations (100 μM) of the ganglionic antagonists d-tubocurarine, mecamylamine and hexamethonium. Equal concentrations of the potent muscle receptor antagonist decamethonium and the competitive antagonist dihydro-β-erythroidine were much less effective. α bungarotoxin (1 μM) had little effect on ACh-induced responses. This physiological and pharmacological profile is consistent with a ganglionic nicotinic response.

Original languageEnglish
Pages (from-to)101-109
Number of pages9
JournalMolecular Brain Research
Issue number1
StatePublished - Jan 1995


  • Agonist efficacy
  • Agonist potency
  • Desensitization
  • Ganglionic antagonists
  • Muscarinic receptor
  • Nicotinic receptor expression
  • α Bungarotoxin


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