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Gustavo Murer"Cortical control of basal ganglia activity in a rat model of Parkinson disease."

Abstract :


Processing of cortical input in the basal ganglia depends on the integrity of the nigrostriatal dopaminergic pathway.
The main clinical manifestations of Parkinson's disease are caused by modifications of basal ganglia activity, which are linked to the progressive loss of mesencephalic dopaminergic neurons. In a rat model of Parkinson's disease we have studied cortical control of basal ganglia activity in vivo under anesthesia. In parkinsonism: i) neurons in the striatum, globus pallidus (GP) and substantia nigra pars reticulata (SNr) exaggeratedly encode cortical slow waves; ii) neurons in the striatum, SNr and GP show an increased probability of responding with an excitation to cortical stimulation; iii) stimulation of dopamine receptors reduces abnormal fast excitations but have little effect on abnormal slow oscillations in the striatum and SNr; iv) rats with moderate forelimb akinesia and partial nigrostriatal damage show abnormal responses to cortical stimulation but spared slow wave control of GP activity. Therefore, cortex-driven low frequency synchronization of basal ganglia activity is related to severe parkinsonism. We hypothesize that it contributes to long term functional changes in the circuit giving rise to clinical signs that do not respond to dopamine replacement therapy. Cortex-driven fast excitations may be more closely related to akinesia since they are present with moderate degrees of nigrostriatal damage and respond to acute stimulation of dopamine receptors.

François Gonon