Abstract

Fractions enriched in astrocytes and nerve-terminals have been isolated from cerebral tissues. The GABA metabolism, the uptake and release of 3H-GABA and its ionic requirements have been studied. The relative activities of γ-aminobutyric acid-α-ketoglutarate transaminase (GABA-T) and glutamic acid decarboxylase (GAD) suggest GABA formation in the nerve terminal and breakdown in the astrocyte. The transport system for 3H-GABA present in the nerve and glia is in our hands undistinguishable, both cells utilizing the membrane potential in combination with the Na +-gradient as the driving force. The low GABA levels in the astrocyte, together with its high membrane-potential, make this cell very suitable to serve a transmitter sink at the GABA synapse. Since 3H-GABA transport in astrocytes seems to be reversible, and since the transport systems in glia and neurons show no characteristic differences, the release of 3H-GABA from synaptosomes has been studied. It is suggested that at least 60–70% of the potassium-evoked release of 3H-GABA in the presence of Ca 2+ is non-vesicular, i.e. does not depend on exogenous Ca 2+.

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