Ethylenediamine as a GABA agonist: Enhancement of diazepam binding and interaction with GABA receptors and uptake sites

Abstract

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]β-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 β-alanine than to GABA.