Ethylenediamine as a GABA agonist: enhancement of diazepam binding and interaction with GABA receptors and uptake sites.
Ethylenediamine (EDA) acted as a GABA agonist by enhancing [3H]diazepam binding to well-washed rat forebrain membrane preparations in a bicuculline-sensitive manner, although its potency was 700-800 times less than that of GABA. EDA was over 3750 times weaker than GABA as a displacer of [3H]GABA bound to membrane receptors and was over 40-fold weaker than GABA at [3H]GABA uptake sites. Its most potent action was as an inhibitor of [3H]beta-alanine uptake into rat cerebral cortex slices. Thus, EDA may show some selectivity for glial rather than neuronal GABA uptake. These data suggest that EDA is a very weak GABA agonist in these in vitro systems and are consistent with EDA bearing a closer structural resemblance to beta-alanine than to GABA.
D000818:Animals; D001665:Binding Sites / Q000187:drug effects*; D001921:Brain / Q000033:anatomy & histology / Q000378:metabolism; D002540:Cerebral Cortex / Q000378:metabolism; D003975:Diazepam / Q000378:metabolism*; D005029:Ethylenediamines / Q000494:pharmacology*; D018756:GABA Antagonists; D008566:Membranes / Q000378:metabolism; D051381:Rats; D011919:Rats, Inbred Strains; D011955:Receptors, Drug / Q000378:metabolism*
D005029:Ethylenediamines; D018756:GABA Antagonists; D011955:Receptors, Drug; C031234:ethylenediamine; D003975:Diazepam