Motility, rigidity and turnover of dopamine in the striatum after administration of morphine to rats: a re-evaluation of their mechanisms.

Whether the delayed behavioural activation and the increase in dopamine (DA) turnover in the striatum reflect signs of rebound effects or of counter-regulatory processes directed against locomotor depression and/or muscular rigidity was studied in rats. Administration of a large dose of morphine (30 mg/kg i.p.) induced strong muscular rigidity, which was measured as tonic activity in the electromyogram (EMG). This effect was maximal after one hour and disappeared during the fourth hour. The locomotor activity, on the other hand, disappeared after 30 min and re-appeared during the fourth hour, followed by a locomotor stimulation with a maximum after 4.5 hr. Striatal lesions produced with kainic acid did not affect the complete locomotor depression (akinesia), except by slightly prolonging this effect, and did not influence the delayed locomotor stimulation. These lesions did not inhibit, but, on the contrary, enhanced the increase in striatal concentration of 3,4-dihydroxyphenylacetic acid (DOPAC). Injections of morphine (10 micrograms) into the substantia nigra led to an increase in the level of DOPAC in the ipsilateral, but not the contralateral striatum. These results, in conjunction with those of other authors, suggest that the increase in DA turnover in the striatum and the delayed locomotor stimulation ought to be regarded as actions of morphine on sites different from those mediating muscular rigidity.