Presence of Radiolabelled Metabolites in Release Studies Using [3H]γ‐Aminobutyric Acid

Abstract
Most studies on γ‐aminobutyric acid (GABA) release from nervous tissue have been conducted using radiolabelled GABA in the presence of aminooxyacetic acid (AOAA) to inhibit GABA: 2‐oxoglutarate aminotransferase (GABA‐T) to prevent conversion of labelled GABA to labeled catabolites. Here we present data showing that even in the presence of 10 μM‐AOAA the spontaneous release of tritium from rat cortical synaptosomes prelabelled with 2,3‐[3H]GABA is mainly in the form of tritiated water but that the increase in tritium release in the presence of unlabelled GABA or high potassium‐ion concentrations is in the form of authentic [3H]GABA. Interpretation of results should take these facts into account.