Hypokinetic disorders result from overactivity in the indirect pathway.
example: Decreased level of dopamine supply in nigrostriatal pathway results in akinesia, bradykinesia, and rigidity in Parkinson’s dieseas (PD).
Hyperkinetic disorders result from underactivity in the indirect pathway.
example: Lesions of STN result in Ballism. Damage to the pathway from Putamen to GPe results in Chorea, both of them are involuntary limb movements.
Lesion-making in STN or GPi are successful therapeutic procedures of PD.
Putamen, GPi, and GPe are organized somatotopically. Their neurons are selectively responsive to the direction of limb movement. A considerable convergence is also evident along the cortico-basal ganglio- thalamo- cortical pathway.
GPi cells have a baseline firing rate of 60-80Hz.
During a voluntary hand movement, the firing rates of 70% of the cells in the hand area of GPi increase, while those of the remaining 30% decrease.
Focusing theory vs. Scaling theory ( result of emphasis on somatotopy vs. convergence)
New findings inconsistent with the old model
Most striatal cells have both D1 and D2 receptors.
GPe neurons send some axons back to striatum.
Although the projections from GPe to GPi are inhibitory, the pattern of activity in GPe replicates that of GPi (the 70-30 distribution of increase/decrease in firing rate).
STN neurons project strongly back to GPe.
SNc send dopaminergic projections to GPe, GPi, and STN.
Intralaminar group of thalamic nuclei, receive projections from GPi and send projections to Putamen. This is some sort of feedback.