Linked Life Data

15359086

Source:http://linkedlifedata.com/resource/pubmed/id/15359086

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2004-9-22
pubmed:abstractText
Carbachol (CCh) caused a dose-dependent release of beta-hexosaminidase and an increase in the production of inositol 1,4,5-trisphosphate (IP3) in RBL-2H3 cells transfected with m2 mAChR cDNA (RBL-m2 cells). The secretion was completely inhibited by LaCl3 and pertussis toxin. The secretion was dependent on extracellular Ca2+ and mediated through the pertussis toxin-sensitive G protein. Exposing RBL-m2 cells to 100 microM CCh for 30 min in Ca2+ -free medium (desensitizing treatment) inhibited the secretion induced by the subsequent addition of 10 microM CCh plus Ca2+, but not by stimulating the high affinity IgE receptor (FcepsilonRI). Desensitizing treatment of RBL-m2 cells reduced the affinity of the lipophilic ligand [3H]quinuclidinyl benzilate to m2 mAChR without a reduction of the total m2 mAChR number. The treatment also decreased the cell surface mAChR number to 14% with a slight reduction in its affinity. Desensitizing treatment of RBL-m2 cells inhibited the CCh-induced transient increase in levels of IP3 and intracellular Ca2+ concentration. The results suggested that the CCh-induced desensitization of m2 mAChR-mediated secretion is due to the receptor sequestration followed by blocking the increase in [Ca2+]i and that this desensitizing mechanism is receptor-subtype-specific.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
1347-8613
pubmed:author
pubmed:issnType
Print
pubmed:volume
96
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
73-83
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
2004
pubmed:articleTitle
Carbachol-induced secretion and homologous desensitization in rat basophilic leukemia (RBL-2H3) cells transfected with human m2 muscarinic acetylcholine receptors.
pubmed:affiliation
Department of Pharmacology, Meiji Pharmaceutical University, Kiyose, Tokyo, Japan. oishikz@my-pharm.ac.jp
pubmed:publicationType
Journal Article, Comparative Study