Physostigmine modulation of acetylcholine currents in COS cells transfected with mouse muscle nicotinic receptor
Language English Country Ireland Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
16530961
DOI
10.1016/j.neulet.2006.02.065
PII: S0304-3940(06)00223-0
Knihovny.cz E-resources
- MeSH
- Acetylcholine metabolism pharmacology MeSH
- Cell Membrane drug effects genetics metabolism MeSH
- Chlorocebus aethiops MeSH
- Cholinesterase Inhibitors pharmacology MeSH
- COS Cells MeSH
- Physostigmine pharmacology MeSH
- Genetic Vectors genetics MeSH
- Ion Channels drug effects genetics metabolism MeSH
- Muscle, Skeletal innervation metabolism MeSH
- Membrane Potentials drug effects genetics MeSH
- Patch-Clamp Techniques MeSH
- Mice MeSH
- Neuromuscular Junction drug effects metabolism MeSH
- Synaptic Transmission drug effects genetics MeSH
- Receptors, Nicotinic drug effects genetics metabolism MeSH
- Drug Synergism MeSH
- Transfection MeSH
- Dose-Response Relationship, Drug MeSH
- Animals MeSH
- Check Tag
- Mice MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Acetylcholine MeSH
- Cholinesterase Inhibitors MeSH
- Physostigmine MeSH
- Ion Channels MeSH
- Receptors, Nicotinic MeSH
Physostigmine (Phy), a reversible inhibitor of acetylcholine (ACh) esterase (AChE), may also act as a low potency agonist and a modulator of the nicotinic receptor. The actions of Phy on mouse muscle nicotinic receptors in the COS-7 cell line were studied by the patch-clamp technique. Currents were recorded in the whole-cell mode 3-7 days after cell transfection by plasmids coding alphabetagammadelta combination of receptor subunits. The application of ACh to cells clamped at -10 mV produced inward currents which displayed desensitization. The application of Phy in concentrations up to 1 x 10(-3) M did not give reliable specific whole-cell membrane responses. The application of Phy in concentrations of 10(-6)-10(-4) M together with ACh modulated the amplitude; accelerated desensitization of currents induced by ACh and increased the final extent of desensitization in a concentration-dependent manner. This finding is in contrast to the suppression and slowing down of desensitization by Phy and 1-methyl-galanthamine observed in Torpedo receptors.
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