Linked Life Data

7693498

Source:http://linkedlifedata.com/resource/pubmed/id/7693498

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1993-12-17
pubmed:abstractText
Effects of tetraethylammonium ions on 5-hydroxytryptamine3 (5-HT3) receptor-mediated ion current have been studied in whole-cell voltage clamped N1E-115 cells. Inward currents evoked by superfusion with 10 microM 5-HT are rapidly blocked by external tetraethylammonium and the kinetics of the partially blocked inward currents are slowed down. External tetraethylammonium also prevents, but is unable to reverse, agonist-induced desensitization of the 5-HT3 receptor-mediated ion current. Both effects depend on tetraethylammonium concentration and attain half maximum values at 2.6-2.8 mM tetraethylammonium. Tetraethylammonium acts externally, since substituting internal monovalent cations by 107 mM tetraethylammonium fails to block 5-HT3 receptor-mediated ion current. This ion substitution causes a shift in the current reversal potential towards a more positive value, indicating that the receptor-operated ion channel is permeable to tetraethylammonium. An IC50 effect of external tetraethylammonium is reduced to 28% blockade when currents are evoked by 50 microM instead of 10 microM 5-HT, indicating that tetraethylammonium and 5-HT compete for the same site. It is concluded that tetraethylammonium shows low affinity for (part of) the agonist binding site involved in the activation as well as in the desensitization of the receptor-operated ion channel.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0014-2999
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
246
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
247-54
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1993
pubmed:articleTitle
Tetraethylammonium ions block 5-HT3 receptor-mediated ion current at the agonist recognition site and prevent desensitization in cultured mouse neuroblastoma cells.
pubmed:affiliation
Research Institute of Toxicology, Utrecht University, The Netherlands.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't