Alterations in local cerebral glucose utilization (LCGU) in rats with unilateral striatal lesions and the modification by apomorphine were investigated. Electrolytic lesions were made in the rostral part of the right striatum, and 1, 7, and 30 days later, LCGU was observed in terms of relative and absolute LCGU values, using the [14C]deoxyglucose method. A definite change in the pattern of LCGU was seen only at 7 days. These were increases in LCGU in the globus pallidus, entopeduncular nucleus and substantia nigra pars reticulata, and decreases in the ventroanterior-ventrolateral (VAL) and ventromedial (VM) thalamic nuclei and lateral habenula, all on the lesioned side. The circling behavior following the lesion, however, was maximal after 2 days and disappeared after 7 days. Intravenous administration of apomorphine (1.5 mg/kg) produced different modifications in the LCGU pattern between the intact and lesioned sides, at 7 days after producing the lesions. On the intact side, there were increases in LCGU in the striatum, globus pallidus, entopeduncular nucleus, substantia nigra pars reticulata and subthalamic nucleus, and a decrease in the lateral habenula. No such changes were observed on the lesioned side. These results indicate firstly that electrolytic striatal lesions induce LCGU increases or decreases in the structures which receive the striatal input, secondly that the mechanism of this change differs from that of the circling behavior seen in case of striatal lesions, and finally that the majority of the LCGU changes in the basal ganglia and thalamus following intravenous administration of apomorphine are brought about by an altered input of neuronal activity from the striatum to these structures.
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