L. P. Davies, J. Hambley, G. Johnston
Mar 17, 1982
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Journal
Neuroscience Letters
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]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.