1 The effect of purine compounds on the potassium-evoked release of '4C-labelled y-aminobutyric acid (GABA) has been studied in 400 gm slices of rat cerebral cortex in vitro. 2 Adenosine and adenosine 5' monophosphate (AMP) inhibited the release of GABA at 10-5 to 10-' M. Adenosine triphosphate (ATP) produced a significant inhibition of release only at 10-' M.3 Theophylline i0-' or 10'-M reduced the inhibitory effect of adenosine, but did not change basal release of GABA. 4 Dipyridamole 10'5 M itself reduced evoked GABA release, but did not prevent the inhibitory effect of adenosine, implying that adenosine was acting at an extracellularly directed receptor. 5 Calcium removal or antagonism by verapamil reduced the evoked release of GABA, but adenosine did not produce any further reduction of the calcium-independent release. This may indicate that the inhibitory effect of adenosine on GABA release results from interference with calcium influx or availability within the terminals.

1. The characteristics of the release of adenosine have been examined from slices of rat cerebral cortex after incubation with [3H]adenine or [3H]adenosine. 2. Increasing the potassium concentration of the extracellular medium to 36 or 54 mM did not evoke any release, but release was observed in the first post‐potassium sample. This occurred whether potassium was present for 2 or 10 min. 3. Calcium‐free solutions or verapamil prevented the post‐potassium release of tritium. Tetraethylammonium bromide and 4‐aminopyridine had no effect. 4. Ouabain (100 microM) induced the release of tritium, and did not prevent an additional increment of release after potassium stimulation. Ouabain induced release did not occur in calcium‐free or sodium‐free media, but was increased in low calcium (0.1 mM) medium. 5. It is concluded that the characteristics of adenosine release are unlike those of conventional neurotransmitters. It is suggested that the release is associated with the influx of sodium and calcium ions through sodium channels.

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