EEG modifications in the cortex and striatum after dopaminergic priming in the 6-hydroxydopamine rat model of Parkinson's disease.

In rats bearing a unilateral 6-hydroxydopamine (6-OHDA) lesion of the medial forebrain bundle, a single administration of a dopamine receptor agonist (priming) sensitizes the behavioral motor responses to a dopaminergic agonist, administered 3 days after priming. In this study, changes in the electroencephalogram (EEG) frequency spectra were evaluated during priming in unilaterally 6-OHDA-lesioned rats, implanted bilaterally with electrodes both in the somatosensory cortex and striatum. Two weeks after 6-OHDA lesion, rats were primed with apomorphine (0.2 mg/kg) and received a challenge with the D(1) agonist SKF 38393 (3 mg/kg) 3 days later. 6-OHDA lesion modified the EEG pattern mainly in the beta(1) frequency band, in both cortex and striatum. Apomorphine priming produced a power decrease in the beta(1) frequency band, more pronounced in the cortex than in the striatum, as compared to saline-treated rats. Antagonism of NMDA receptor with MK-801, a treatment known to block the development of priming, increased apomorphine inhibitory effect mainly in the striatum, producing the same degree of inhibition in the two structures. Administration of SKF 38393, 3 days after priming, caused a power decrease in beta(1) frequency band of the cortex and striatum, which was more pronounced in apomorphine-primed as compared to drug-naive rats. The inhibitory effect of SKF 38393 was enhanced in rats primed with MK-801 plus apomorphine, particularly in the striatum. The results of this study suggest that long-term changes in the electrical activity of cortex and striatum after priming, might contribute to the development of the behavioral sensitization observed after priming. Development of priming might be related to the degree and cortical/striatal ratio of EEG power inhibition produced by dopamine agonists.