Lack of morphine-induced hyperactivity in C57BL/6 mice following striatal kainic acid lesions.

Bilateral injection of kainic acid (0.15 micrograms/0.3 microliters) into the striatum (caudatus/putamen) of C57BL/6 mice prevented stimulation of locomotor activity by morphine (20 mg/kg, i.p.). This effect was specific to morphine since mice with the same lesion did not show any impairment of amphetamine (2 mg/kg)-induced locomotor hyperactivity. Histological inspections showed neuron damage also in the nucleus accumbens, while hippocampus was not damaged by kainic acid. Moreover, mice with kainic acid lesions in the hippocampus were more stimulated by morphine, compared with the morphine-injected sham lesion group. The results, which suggest the existence of non-catecholaminergic mediations in the locomotor effects of morphine, are discussed in terms of opioid systems in the brain.