Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1981-12-22
pubmed:abstractText
This study describes effects of ACTH1-24 and beta-endorphin on brain polyphosphoinositide metabolism in vitro. The interconversion of these polyanionic phospholipids was studied by incubation of a lysed synaptosomal fraction with [gamma-32P]ATP. Of the membrane phospholipids only PA, DPI and TPI became labeled. The reference peptide ACTH1-24 stimulated the formation of TPI and inhibited the production of PA. For effects on TPI formation both the sequences ACTH5-7 and ACTH10-16 were needed. Effects on PA formation required the sequences ACTH7-10 and ACTH10-16. The basic amino acids in ACTH10-16 seemed to be of crucial importance for the peptide effects. A stimulatory effect on DPI was visible when ACTH was shortened from the N-terminus, and the essential information was in ACTH7-10. beta-endorphin inhibited PA formation and this effect was abolished by C-terminal shortening to gamma-endorphin. Other fragments of the C-terminus of beta-LPH, including the enkephalins, were ineffective. It is concluded that the structure-activity relationship on TPI/PA formation correlates with a similar relationship obtained on excessive grooming behavior in vivo. A possible correlation between the effects on polyPI metabolism and opiate-like effects, and effects on extinction of active avoidance behavior in vivo is discussed.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0006-8993
pubmed:author
pubmed:issnType
Print
pubmed:day
16
pubmed:volume
224
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
315-26
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
1981
pubmed:articleTitle
Modulation of brain polyphosphoinositide metabolism by ACTH and beta-endorphin: structure-activity studies.
pubmed:publicationType
Journal Article