Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1998-6-18
pubmed:abstractText
Neuronal alpha1E Ca2+ channels were expressed in Xenopus laevis oocytes alone and in combination with the mu opioid receptor. Macroscopic currents were recorded under voltage clamp conditions. The stimulation of the morphine receptor by the synthetic [D-Ala2,N-Me-Phe4,Gly-ol5] enkephalin (DAMGO) produced a 20% reduction in the alpha1E ionic current. This effect was associated with a large change in the decay phase of the Ba2+ current. The effect of 1 microM DAMGO was fully antagonized by the universal mu opioid receptor antagonist naloxone and by the selective antagonist beta-funaltrexamine. The ionic current inhibition induced by DAMGO was partially recovered by preceding strong depolarizations. The injection of the catalytic subunit of pertussis toxin (A-protomer) abolished the effect of DAMGO, suggesting the involvement of a GTP binding protein in the alpha1E modulation. The coexpression of the regulatory beta2a Ca2a channel subunit, together with the alpha1E subunit and the mu opioid receptor, prevented the reduction of the ionic current following the receptor stimulation with DAMGO, whereas the coexpression with the beta3 subunit reduced by approximately 50% the modulatory effect of DAMGO. The effect produced by the stimulation of the opioid receptor could be mimicked by coexpressing the alpha1E channel with the G-protein betagamma subunits.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0014-5793
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
427
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
96-102
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1998
pubmed:articleTitle
Functional coupling between human E-type Ca2+ channels and mu opioid receptors expressed in Xenopus oocytes.
pubmed:affiliation
Department of Anesthesiology, University of California Los Angeles, 90095-1778, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't