The effect of pharmacological stimulation of the amygdala on spontaneous locomotor activity in the rat and its modulation by accumbens dopamine were investigated. Bilateral injection of N-methyl-D-aspartic acid into the basolateral nucleus of the amygdala produced a dose-dependent suppression of spontaneous locomotor activity in the rat. The suppression of locomotor activity was reversed completely by injection of L-glutamic acid diethyl ester, a putative glutamatergic antagonist, into the nucleus accumbens but partially enhanced by injection of nipecotic acid, a GABA uptake inhibitor, into the ventral pallidum. Furthermore, low doses of dopamine injected into the accumbens, which by itself did not elicit hyperactivity in the animals, completely reversed the suppression of locomotor activity following amygdala stimulation. These results show that the projection from the amygdala to nucleus accumbens has an inhibitory effect on spontaneous locomotor activity in rats and that dopamine in the accumbens attenuated this suppression effect possibly due to its neuromodulatory action as demonstrated in previous electrophysiological experiments.