A carrier for GABA uptake exists on noradrenaline nerve endings in selective rat brain areas but not on serotonin terminals

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Abstract
γ-Aminobutyric acid (GABA) increased in a concentration-dependent way (3–300ΜM) the basal release of tritium from rat cerebral cortex and hippocampus synaptosomes, prelabelled with3H-noradrenaline (3H-NA); however, GABA was ineffective on hypothalamic nerve endings. The effect displayed by low concentrations (ΜM) of GABA was largely bicuculline-sensitive. Muscimol mimicked GABA, while (−)baclofen was inactive. The releasing effects produced by concentrations of GABA higher than 10ΜM were largely prevented by SK&F89976A, SK&F 100330A and SK&F 100561, three novel GABA uptake inhibitors. When present together, GABA uptake blocker and bicuculline counteracted entirely the GABA effects. The basal release of3H-5-hydroxytryptamine (3H-5-HT) in synaptosomes from various CNS regions was not affected by GABA. In conclusion: GABA can enhance3H-NA release not only through GABA-A receptors but also by penetrating into NA terminals through a GABA uptake system. This implies coexistence of carriers for NA and GABA uptake on a same nerve terminal. The carrier coexistence occurs in selective CNS areas. The phenomenon appears to be transmitter-selective.