Linked Life Data

6330299

Source:http://linkedlifedata.com/resource/pubmed/id/6330299

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1984-8-8
pubmed:abstractText
Dopamine and dopamine receptor agonists were found to inhibit adenylate cyclase activity dose-dependently in a neuroblastoma X Chinese hamster brain explant hybrid cell line NCB-20. Apomorphine (with an IC50 value of 10 nM) was the most effective inhibitor, followed by 2-amino-6,7-dihydroxy-1,2,3,4-tetrahydronaphthaline (ADTN), dopamine, and N-dipropyldopamine. The inhibition was potently reversed by sulpiride, butaclamol, and flupenthixol in a stereospecific manner, but was unaffected by yohimbine, except at high concentrations. Clonidine also inhibited adenylate cyclase activity in these cells and this was reversed by the alpha 2-adrenoreceptor antagonist yohimbine, but not by sulpiride. [D-Ala2, D-Leu5] Enkephalin inhibited adenylate cyclase activity in NCB-20 cells at nanomolar concentrations; this was reversed by naloxone. All three inhibitory neurotransmitters were able to reverse the stimulation of cyclic AMP synthesis by serotonin or prostaglandin E1. The dopamine receptor that modulates cyclic AMP synthesis in NCB-20 cells is pharmacologically quite distinct from a high-affinity spiperone binding site identified in these cells, but shows the pharmacologic specificity of the "D2" receptor previously described in mammalian brain.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0022-3042
pubmed:author
pubmed:issnType
Print
pubmed:volume
43
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
413-20
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1984
pubmed:articleTitle
Specific receptor-mediated inhibition of cyclic AMP synthesis by dopamine in a neuroblastoma X brain hybrid cell line NCB-20.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't