Linked Life Data

11738029

Source:http://linkedlifedata.com/resource/pubmed/id/11738029

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2001-12-12
pubmed:abstractText
Morphine is unusual in its failure to promote robust desensitization and endocytosis of the mu opioid receptor (MOR), processes that for many receptors contribute directly to tolerance. This apparent paradox has led us to revise the idea that receptor desensitization and endocytosis are solely responsible for tolerance and withdrawal to morphine, and instead test the hypothesis that these side effects occur due to abnormally prolonged MOR signaling. We report here that MOR mutations that facilitate endocytosis reduce the development of cellular tolerance and cAMP superactivation, a cellular hallmark of withdrawal. Moreover, mutant receptors with reduced endocytosis produce exacerbated superactivation. These data demonstrate a critical role for receptor endocytosis in the development of adverse side effects associated with prolonged opiate use.
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0896-6273
pubmed:author
pubmed:issnType
Print
pubmed:day
6
pubmed:volume
32
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
829-39
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2001
pubmed:articleTitle
Endocytosis of the mu opioid receptor reduces tolerance and a cellular hallmark of opiate withdrawal.
pubmed:affiliation
Department of Molecular and Cell Biology, University of California, Berkeley, CA 94720, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't