期刊名称：Proceedings of the National Academy of Sciences
印刷版ISSN：0027-8424
电子版ISSN：1091-6490
出版年度：1998
卷号：95
期号：24
页码：14184-14189
DOI：10.1073/pnas.95.24.14184
语种：English
出版社：The National Academy of Sciences of the United States of America
摘要：Methyllycaconitine (MLA), -conotoxin ImI, and -bungarotoxin inhibited the release of catecholamines triggered by brief pulses of acetylcholine (ACh) (100 {micro}M, 5 s) applied to fast-superfused bovine adrenal chromaffin cells, with IC50s of 100 nM for MLA and 300 nM for -conotoxin ImI and -bungarotoxin. MLA (100 nM), -conotoxin ImI (1 {micro}M), and -bungarotoxin (1 {micro}M) halved the entry of 45Ca2+ stimulated by 5-s pulses of 300 {micro}M ACh applied to incubated cells. These supramaximal concentrations of 7 nicotinic receptor blockers depressed by 30% (MLA), 25% (-bungarotoxin), and 50% (-conotoxin ImI) the inward current generated by 1-s pulses of 100 {micro}M ACh, applied to voltage-clamped chromaffin cells. In Xenopus oocytes expressing rat brain 7 neuronal nicotinic receptor for acetylcholine nAChR, the current generated by 1-s pulses of ACh was blocked by MLA, -conotoxin ImI, and -bungarotoxin with IC50s of 0.1 nM, 100 nM, and 1.6 nM, respectively; the current through 3{beta}4 nAChR was unaffected by -conotoxin ImI and -bungarotoxin, and weakly blocked by MLA (IC50 = 1 {micro}M). The functions of controlling the electrical activity, the entry of Ca2+, and the ensuing exocytotic response of chromaffin cells were until now exclusively attributed to 3{beta}4 nAChR; the present results constitute the first evidence to support a prominent role of 7 nAChR in controlling such functions, specially under the more physiological conditions used here to stimulate chromaffin cells with brief pulses of ACh.
