Noncompetitive inhibition by camphor of nicotinic acetylcholine receptors

The effect of camphor, a monoterpenoid, on catecholamine secretion was investigated in bovine adrenal chromaffin cells. Camphor inhibited [H-3]norepinephrine ([H-3]NE) secretion induced by a nicotinic acetylcholine receptor (nAChR) agonist, 1,1-dimethyl-4-phenylpiperazinium iodide (DMPP), with a half-maximal inhibitory concentration (IC50) of 70 +/- 12 muM. In addition, camphor inhibited the rise in cytosolic calcium ([Ca2+](i)) and sodium ([Na+](i)) induced by DMPP with IC50 values of 88 +/- 32 and 19 +/- 2 muM, respectively, suggesting that the activity of nAChRs is also inhibited by camphor. On the other hand, binding of [H-3]nicotine to nAChRs was not affected by camphor. [Ca2+](i) increases induced by high K+, veratridine, and bradykinin were not affected by camphor. The data suggest that camphor specifically inhibits catecholamine secretion by blocking nAChRs without affecting agonist binding. (C) 2001 Elsevier Science Inc. All rights reserved.