Article date: 1988/1/1
PubMed ID: 2898899
Journal name: Brain & development (ISSN: 0387-7604)
The effects of ACTH4-10 and ACTH1-24 on L-[3H]glutamate (Glu) binding sites and GABA/benzodiazepine/picrotoxin receptor complexes in vitro were investigated. ACTH4-10 and ACTH1-24 inhibited [3H] Glu and [3H] muscimol binding concentration-dependently, while [3H] flunitrazepam (FNP) and [35S] t-butylbicyclophosphorothionate (TBPS) binding were not affected. These ACTH fragments also inhibited GABA-stimulated [3H] FNP binding. These results suggest that ACTH and its fragments may act as anticonvulsants by antagonizing glutamate binding, their interaction with GABA-A sites may relate to the other central nervous effects of ACTH than the anticonvulsant activity.
Author List: Ito M, Yu O, Chiu T H
Publication Types: Journal Article; Research Support, U.S. Gov't, P.H.S.
Substances mentioned in the article: Bridged Bicyclo Compounds; Bridged Bicyclo Compounds, Heterocyclic; Glutamates; Peptide Fragments; Receptors, GABA-A; Receptors, Glutamate; Receptors, Neurotransmitter; picrotoxinin receptor; Muscimol; Glutamic Acid; Flunitrazepam; tert-butylbicyclophosphorothionate; Adrenocorticotropic Hormone; ACTH (4-10);
Mesh terms: Adrenocorticotropic Hormone/metabolism; Animals; Binding Sites; Bridged Bicyclo Compounds/metabolism; Bridged Bicyclo Compounds, Heterocyclic; Cerebral Cortex/metabolism; Flunitrazepam/metabolism; Glutamates/metabolism; Glutamic Acid; Male; Muscimol/metabolism; Peptide Fragments/metabolism; Rats; Rats, Inbred Strains; Receptors, GABA-A/metabolism; Receptors, Glutamate; Receptors, Neurotransmitter/metabolism;