Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1997-6-19
pubmed:abstractText
n-Alkyl sulphate anions have been shown to reversibly affect the functioning of voltage-gated ion channels in a variety of preparations. They are suggested to exert their effects by increasing the magnitude of the negative surface potential at the external face of the membrane. Here we report the effects of n-octyl sulphate (OS-) and n-dodecyl sulphate (DDS-) on RCK1 (Kv1.1), RCK4 (Kv1.4) and Shaker B potassium channels exogenously expressed in Xenopus oocytes. Both OS- and DDS- produced a hyperpolarising shift in the activation voltage dependence of all three channels, consistent with an increased negative external surface potential. Similar kinetic changes were also observed, the kinetics of both activation and inactivation being accelerated in the presence of OS- and DDS-. However, we also found that while 10 mM OS- and 50 microM DDS- significantly increased the maximum conductance of RCK1 and Shaker B channels, 5 mM OS- and 15 microM DDS- produced a large decrease in RCK4 conductance; the possible involvement of RCK4 residue K533 in this effect is discussed. Our data indicate that n-alkyl sulphate anions can perturb ion channel function in a variety of ways and that their effects are complex and channel specific.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0031-6768
pubmed:author
pubmed:issnType
Print
pubmed:volume
434
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
132-6
pubmed:dateRevised
2009-9-29
pubmed:meshHeading
pubmed:year
1997
pubmed:articleTitle
Channel-specific effects of n-alkyl sulphate anions on three shaker-related potassium channels expressed in Xenopus oocytes.
pubmed:affiliation
Department of Anatomy and Physiology, University of Dundee, Dundee DD1 4HN, Scotland, UK.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't