Abstract
GABA potentiates the potassium-evoked release of methionine-enkephalin (ME) from slices of rat corpus striatum. This potentiation is observed only when a submaximal concentration (30 mM) of K + is used to evoke release. The effect of GABA is dose-dependent between 100 and 1000 μM. The basal release of ME is not altered by these concentrations of GABA. Baclofen, but not muscimol, mimics the effect of GABA on the evoked release of ME. This effect is not stereoselective as both the (+)- and (−)-isomers of baclofen enhance ME release. Picrotoxin (100 μM) blocks the enhancement of ME release produced by both GABA and baclofen. Bicuculline methiodide (100 μM) does not block the effect of GABA. The effect of GABA on ME release may be mediated by an atypical GABA receptor which is activated by baclofen.
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