Effects of striatal lesions with kainic acid on morphine-induced "catatonia" and increase of striatal dopamine turnover.

The influence of striatal lesions (head of the caudate nucleus) with kainic acid on "catatonia" and on the increase of the dopamine metabolite DOPAC in the striatum after systemic morphine administration was measured in rats. These lesions strongly prevented the morphine-induced muscular rigidity, measured as activity in the electromyogram EMG) of the gastrocnemius-soleus muscle of non-anesthesized animals. On the other hand, the decrease of locomotion (akinesia) measured using an Animex Activity Meter and an activity wheel, was not prevented or reduced. The lesions did not influence the inhibitory effect of morphine on the activation of flexor alpha-motoneurones, either. These results suggest that the head of the caudate nucleus plays an important role in mediating morphine rigidity, but not akinesia or inhibition of the activation of flexor alpha-motoneurones. Opioid-induced "catatonia" ought to be regarded as a mixture both of rigidity and of akinesia. Morphine led to a rapid decrease, followed by a slow increase of striatal DOPAC concentration. Lesions induced by kainic acid slightly inhibited the decrease and markedly enhanced the increase of DOPAC. Accordingly, an intact nigro-striato-nigral loop is not necessary for the increase of striatal dopamine turnover, observed after morphine administration. The different sites of action, which are likely to mediate all these effects of morphine, are discussed.