Article date: 1989/12/1
PubMed ID: 2575438
Journal name: Brain research bulletin (ISSN: 0361-9230)
The peptides MIF-1 (Pro-Leu-Gly-NH2) and Tyr-MIF-1 (Tyr-Pro-Leu-Gly-NH2) recently have been found to augment the effects of gamma-aminobutyric acid (GABA) on benzodiazepine receptor binding and chloride channel binding (Tyr-MIF-1) at the GABAA receptor complex. To determine whether these peptides affect the function of this complex in chloride transport, we evaluated chloride uptake stimulated by the GABA analog muscimol in synaptoneurosome preparations. In mice treated with either MIF-1 or Tyr-MIF-1 (1 mg/kg IP), maximal chloride uptake in cortex was increased compared with controls. The two peptides had similar effects in cortical preparations, but in cerebellum neither peptide altered chloride uptake. No differences from controls were observed in cortical synaptoneurosomes treated in vitro with either MIF-1 or Tyr-MIF-1. These results suggest that the brain peptides MIF-1 and Tyr-MIF-1 alter function at the GABAA receptor complex, perhaps by binding at a specific peptide 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.; Research Support, U.S. Gov't, P.H.S.
Substances mentioned in the article: Chlorides; Receptors, GABA-A; Muscimol; tyrosyl-prolyl-leucyl-glycinamide; MSH Release-Inhibiting Hormone;
Mesh terms: Animals; Cerebral Cortex/drug effects; Chlorides/pharmacokinetics; MSH Release-Inhibiting Hormone/analogs & derivatives; Male; Mice; Muscimol/pharmacology; Receptors, GABA-A/drug effects;