Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
1988-4-15
pubmed:abstractText
The peptides Tyr-MIF-1 (Tyr-Pro-Leu-Gly-NH2) and, to a lesser extent, MIF-1 (Pro-Leu-Gly-NH2) recently have been found to augment the effects of gamma-aminobutyric acid (GABA) on benzodiazepine receptor binding at the GABAA receptor complex. To assess their interaction with the chloride channel binding site on the GABAA receptor, we evaluated the effects of these two peptides on [35S]-t-butylbicyclophosphorothionate (TBPS) binding in mouse brain membranes. In cortex, neither peptide altered [35S]-TBPS binding over a broad dose range, but Tyr-MIF-1 significantly augmented displacement of radioligand binding by the GABA analog muscimol at peptide concentrations of 10(-10) to 10(-7) M; MIF-1 had little effect on muscimol displacement of [35S]-TBPS binding. In cerebellum and brainstem, neither peptide was active in altering muscimol displacement of binding. Thus, Tyr-MIF-1 augments the displacement of [35S]-TBPS binding by the GABA analog muscimol in mouse brain cortical membranes, indicating that this peptide enhances the effects of GABA at the chloride channel as well as at the benzodiazepine receptor.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0361-9230
pubmed:author
pubmed:issnType
Print
pubmed:volume
19
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
743-5
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1987
pubmed:articleTitle
Effects of Tyr-MIF-1 and MIF-1 at the GABAA receptor chloride channel site.
pubmed:affiliation
Department of Medicine, LSU Medical Center, New Orleans, LA 70112.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, Non-P.H.S.