Linked Life Data

7752097

Source:http://linkedlifedata.com/resource/pubmed/id/7752097

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1995-6-19
pubmed:abstractText
Opioid sensitivity of a catecholaminergic cell line (CATH.a) of brainstem origin was examined using whole-cell voltage-clamp techniques. Morphine produced a preferential and concentration-dependent decrease of the amplitude of voltage-activated potassium current, IK (ED50 = approximately 4 microM, maximum inhibition 52%, n = 33). The mu-selective opiate agonist [D-Ala2, MePhe, Gly-ol5] enkephalin (2-20 microM; n = 6) and the delta-selective agonist [D-Pen2, D-Pen5] enkephalin (2-20 microM; n = 7) produced no effect. However, the kappa-selective agonist trans-(+/-)-3,4-dichloro-N-methyl-N-(2-[1-pyrrolidinyl]cyclohexyl)ben zene-acetamide reduced IK in a concentration-dependent manner (EC50 = 2.3 microM, maximum inhibition 44%, n = 40). The kappa receptor antagonist nor-binaltorphimine (10 nM) blocked the effect of either morphine (10 microM, n = 6) or U50,488 (10 microM, n = 7). Kappa agonist-mediated IK reduction was prevented by intracellular dialysis with an inactive form of guanosine diphosphate, guanosine 5'-O-(2-thio)diphosphate (100-200 microM; n = 10) but was unchanged by incubation with pertussis toxin (500 ng/ml, 24-48 h, n = 10). These results suggest that opioid suppression of IK is mediated by kappa-opioid receptors coupled to a pertussis toxin-insensitive G-protein.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0022-3565
pubmed:author
pubmed:issnType
Print
pubmed:volume
273
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
927-33
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1995
pubmed:articleTitle
Kappa opioid receptor-mediated suppression of voltage-activated potassium current in a catecholaminergic neuronal cell line.
pubmed:affiliation
Department of Pharmacology, University of Virginia Health Sciences Center, Charlottesville, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.