Abstract
The rate of release of enkephalin from rat striatal slices increased 7–10 fold in response to depolarization by 50 mM potassium ions in vitro. The potassium-evoked release of enkephalins was abolished in a calcium deficient medium. Uptake studies indicated that the potassium-stimulated efflux was not due to the inhibition of an active uptake mechanism for these peptides. These findings provide support for the view that enkephalins may function as neurotransmitters in brain.
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