Impact of slow cortical rhythms on basal ganglia output nuclei activity in experimental parkinsonism

TSENG KY; RIQUELME LA; MURER MG

Advances in Behavioral Biology, volume 52, The Basal Ganglia VII

Kluwer Academic / Plenum Publishers

Lugar: New York; Año: 2002; p. 445 - 454

The classic view of basal ganglia functional organization (Albin et al. 1989; DeLong 1990) suggests that in Parkinson’s disease (PD), the lack of dopamine would lead to hyperactivity of output nuclei neurons. This would be due to an imbalance between the activities of the two main output pathways of the striatum: the direct and the indirect pathway. These two circuits have been assumed to be under the preferential control of excitatory D1-class and inhibitory D2-class dopamine receptors, respectively (Gerfen et al., 1990; Wichmann and DeLong 1996). Thus, output nuclei hyperactivity in PD is expected as the functional consequence of two parallel processes: (i) a reduced activity of the inhibitory direct pathway and; (ii) an increased activity of the subthalamic nucleus (STN). Increased STN activity is assumed to result from desinhibition of striatopallidal neurons and the subsequent reduction in tonic inhibitory input from the globus pallidus (GP) to the STN (DeLong 1990; Gerfen et al. 1990)