PubMed1987
Local cerebral glucose utilization was measured in 21 discrete regions of the rat CNS following unilateral kainic acid lesions of the caudate nucleus, and subsequent pharmacological challenge with GABAergic or dopaminergic agonists. The most pronounced increases in glucose use were observed in those ipsilateral areas of the brain to which the lesioned striatum normally projects (globus pallidus, entopeduncular nucleus and substantia nigra pars reticulata), although several other brain regions with known anatomical connections to the striato-pallido-nigral system were also affected, most notably in the thalamus and epithalamus. These effects were similar to those reported previously from a different group of animals in which the injection protocol was slightly different. The consequences of striatal lesion, in terms of alterations in local rates of glucose use, were attenuated by i.v. administration of the putative GABA agonist, muscimol. In one area, the ventromedial thalamus, glucose use was more markedly affected by muscimol treatment bilaterally in lesioned animals than in intact animals. The consequences of striatal lesions upon the response to the putative dopaminergic agonist apomorphine, were both complex and profound. In some regions (e.g. globus pallidus), striatal lesion eliminated, or masked the normal response to apomorphine. Elsewhere, the apomorphine response, although in evidence, was significantly attenuated by striatal lesion (e.g. entopeduncular nucleus), but in only two brain areas, substantia nigra pars reticulata and ventrolateral thalamus, the apomorphine response was significantly potentiated by striatal lesion. These studies add further weight to the concept of disinhibition, mediated via striatal GABA fibres, as an organizing principle in striatonigral function and indicate a complex interaction of intrinsic GABAergic pathways with dopaminergic systems in the integrated response to stimulation of dopaminergic receptors in the extrapyramidal motor system.