Abstract 1. 1. The role of both novel GABA B and classical GABA A receptors in GAG-induced antinociception was investigated using the tail flick and hot plate tests. To this end, manipulations known to increase baclofen-induced antinociception (GABA B) and the receptor antagonist bicuculline (GABA A) were used. 2. 2. Of the modifiers of monoamine function tested, only chlorpromazine and haloperidol significantly increased GAG-induced antinociception. 3. 3. Theophylline antagonized antinociception produced by both GAG and GVG. 4. 4. Bicuculline did not antagonize antinociception produced by either GAG or muscimol. 5. 5. GAG-induced antinociception does not appear to result from the activation of either classical or novel GABA receptors. An interaction with dopaminergic pathways appears to be involved.