Tunicamycin alters channel gating characteristics of junctional and extrajunctional acetylcholine receptors expressed in Xenopus oocytes.
The acute effects of tunicamycin on mouse junctional and extrajunctional acetylcholine receptors (AChRs) expressed in Xenopus oocytes, distinct from its ability to block N-glycosylation of the protein, was examined at the single channel level. Tunicamycin reduced the frequency of ACh-activated single channel openings and prolonged the mean channel open times of AChRs in a dose-dependent manner, without affecting inward conductances. Continuous application of ACh to both junctional and extrajunctional AChR channels very slowly decreased the number of channel opening events, and tunicamycin accelerated this process. These results suggest that tunicamycin alters channel gating kinetics and accelerates transition towards a desensitized state.
Nishizaki
T
T
Department of Psychobiology, University of California, Irvine 92717-4550.
Sumikawa
K
K
D000818:Animals; D004305:Dose-Response Relationship, Drug; D004594:Electrophysiology; D015640:Ion Channel Gating / Q000187:drug effects*; D007473:Ion Channels / Q000187:drug effects* / Q000502:physiology; D051379:Mice; D009469:Neuromuscular Junction / Q000378:metabolism*; D009865:Oocytes / Q000378:metabolism*; D011950:Receptors, Cholinergic / Q000378:metabolism*; D014415:Tunicamycin / Q000494:pharmacology*; D014981:Xenopus
D007473:Ion Channels; D011950:Receptors, Cholinergic; D014415:Tunicamycin