Linked Life Data

2987487

Source:http://linkedlifedata.com/resource/pubmed/id/2987487

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1985-7-2
pubmed:abstractText
The ability of 5-hydroxytryptamine (5-HT) and related agonists to stimulate hydrolysis of inositol phospholipids was examined in rat cerebral cortex slices using a direct assay which involves prelabeling with [3H]inositol and assaying [3H]inositol phosphates in the presence of lithium. 5-HT agonists stimulated [3H]inositol phosphate accumulation in a dose-related but biphasic manner and only the high-affinity component of the dose-response curve was sensitive to antagonists. This response to 5-HT was blocked potently by ketanserin and other putative 5-HT2 antagonists but the overall pattern of apparent drug affinities was inconsistent with that seen at 5-HT2 sites labeled with [3H]ketanserin in cortical membranes. Pretreatment of slices with the alkylating antagonist phenoxybenzamine reduced the inositol phospholipid response to 5-HT to a greater extent than the suppression of [3H]ketanserin binding. Similarly, chronic but not acute treatment of rats with the antidepressants iprindole and imipramine resulted in a greater loss of 5-HT-induced inositol phospholipid hydrolysis than specific [3H]ketanserin binding. However, the effect of antidepressants was agonist-specific in that neither alpha-1 adrenoceptor nor muscarinic receptor stimulation were altered by acute or chronic treatment.
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
233
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
473-9
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1985
pubmed:articleTitle
5-Hydroxytryptamine-stimulated inositol phospholipid hydrolysis in rat cerebral cortex slices: pharmacological characterization and effects of antidepressants.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't