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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
4
|
| pubmed:dateCreated |
1996-11-5
|
| pubmed:abstractText |
Single channel recordings have shown that ketamine (Ket) decreases the open time of the nicotinic acetylcholine receptor channel (nAChR). The present experiments on simultaneous openings of the nAChRs of mouse myotubes investigate the interaction of Ket with the open as well as with the closed state of the channels. The patch-clamp technique was used to record currents activated by 10(-4) M acetylcholine (ACh) in the outside-out mode. ACh together with increasing concentrations of Ket was applied with a piezo-driven system. In a second protocol, the patches were preexposed to Ket before activation with ACh. With addition of Ket, the currents showed a biexponential decay, indicating an open-channel block. The peak current amplitude decreased reversibly and in a concentration-dependent manner. The rate constants of block (b+1) and of unblock (b-1) were modeled by computer simulation and were found to be: b+1 = 3 x 10(6) M/s, b-1 = 100/s. Preexposure of the patches to Ket revealed an additional block with a KD of approximately 2 x 10(-6) M, which is below clinical concentrations. These data suggest that Ket also interacts with the closed state of the nAChR.
|
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
AIM
|
| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Acetylcholine,
http://linkedlifedata.com/resource/pubmed/chemical/Anesthetics, Dissociative,
http://linkedlifedata.com/resource/pubmed/chemical/Ion Channels,
http://linkedlifedata.com/resource/pubmed/chemical/Ketamine,
http://linkedlifedata.com/resource/pubmed/chemical/Nicotinic Antagonists,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Nicotinic
|
| pubmed:status |
MEDLINE
|
| pubmed:month |
Oct
|
| pubmed:issn |
0003-2999
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
83
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
830-6
|
| pubmed:dateRevised |
2008-11-21
|
| pubmed:meshHeading |
pubmed-meshheading:8831330-Acetylcholine,
pubmed-meshheading:8831330-Anesthetics, Dissociative,
pubmed-meshheading:8831330-Animals,
pubmed-meshheading:8831330-Cells, Cultured,
pubmed-meshheading:8831330-Computer Simulation,
pubmed-meshheading:8831330-Dose-Response Relationship, Drug,
pubmed-meshheading:8831330-Ion Channel Gating,
pubmed-meshheading:8831330-Ion Channels,
pubmed-meshheading:8831330-Ketamine,
pubmed-meshheading:8831330-Membrane Potentials,
pubmed-meshheading:8831330-Mice,
pubmed-meshheading:8831330-Models, Biological,
pubmed-meshheading:8831330-Models, Chemical,
pubmed-meshheading:8831330-Muscle, Skeletal,
pubmed-meshheading:8831330-Muscle Fibers, Skeletal,
pubmed-meshheading:8831330-Nicotinic Antagonists,
pubmed-meshheading:8831330-Patch-Clamp Techniques,
pubmed-meshheading:8831330-Receptors, Nicotinic,
pubmed-meshheading:8831330-Signal Processing, Computer-Assisted
|
| pubmed:year |
1996
|
| pubmed:articleTitle |
Ketamine blocks currents through mammalian nicotinic acetylcholine receptor channels by interaction with both the open and the closed state.
|
| pubmed:affiliation |
Department of Anesthesiology, Technische Universität München, Klinikum rechts der Isar, Munich, Germany.
|
| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|