Direct actions of anticholinesterases on the neuronal nicotinic acetylcholine receptor channels
- Authors
- Nagata, Keiichi; Huang, Chao-Sheng; Song, Jin-Ho; Narahashi, Toshio
- Issue Date
- Sep-1997
- Publisher
- ELSEVIER SCIENCE BV
- Keywords
- anticholinesterase; neostigmine; carbaryl; nicotinic acetylcholine receptor; ion channel; PC12 cell
- Citation
- BRAIN RESEARCH, v.769, no.2, pp 211 - 218
- Pages
- 8
- Journal Title
- BRAIN RESEARCH
- Volume
- 769
- Number
- 2
- Start Page
- 211
- End Page
- 218
- URI
- https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/67062
- DOI
- 10.1016/S0006-8993(97)00707-5
- ISSN
- 0006-8993
1872-6240
- Abstract
- Recent studies have suggested that anticholinesterases including organophosphates and carbamates act directly on the nicotinic acetylcholine receptor (AChR) channel. We performed whole-cell and single-channel patch-clamp experiments to elucidate the mechanism of action of anticholinesterases on the nicotinic AChR in rat clonal phaeochromocytoma (PC12) cells. Neostigmine and carbaryl showed a biphasic effect; enhancement and suppression of carbachol-induced whole-cell currents. The currents induced by 100 mu M carbachol was enhanced by the first co-application with 10 or 100 mu M neostigmine, and the current was eventually suppressed below the control level during repeated co-applications. The decay phase of current was accelerated by neostigmine. Carbaryl at 0.1 mu M greatly potentiated the carbachol-induced current, and at higher concentrations (0.3-3 mu M), current was suppressed. In single-channel experiments, these compounds increased the short closures or gaps during channel opening without changing-the single-channel conductance. Mean open time and burst duration were decreased in the presence of neostigmine and carbaryl. These results indicate that neostigmine and carbaryl directly block the nicotinic AChR channel. (C) 1997 Elsevier Science B.V.
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