Article date: 1987/12/1
PubMed ID: 2449939
Journal name: Brain research bulletin (ISSN: 0361-9230)
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.
Author List: Miller L G, Kastin A J, Roy R B
Publication Types: Journal Article; Research Support, U.S. Gov't, Non-P.H.S.
Substances mentioned in the article: Ion Channels; Receptors, GABA-A; Receptors, Immunologic; macrophage migration inhibitory factor receptor; tyrosyl-prolyl-leucyl-glycinamide; MSH Release-Inhibiting Hormone;
Mesh terms: Animals; Binding, Competitive; Brain/metabolism; Cell Membrane/metabolism; Ion Channels/drug effects; Kinetics; MSH Release-Inhibiting Hormone/analogs & derivatives; Male; Mice; Receptors, GABA-A/drug effects; Receptors, Immunologic/metabolism; Structure-Activity Relationship;