Figure 7

The basal ganglia and cerebellum are involved in motor control. Both circuitries receive projections from the cerebral cortex and send signals to the thalamus. These signals are then accumulated in the cerebral cortex. The inhibitory regulation from the basal ganglia and stimulatory regulation from the cerebellum modulate the activity of the cerebral cortex. UBP141 inhibited the NR2C subunit in both WT and GluN2D KO mice but only inhibited the NR2D subunit in WT mice. Thus, the inhibition of the GluN2D subunit is a more important factor for motor impairment than the inhibition of the GluN2C subunit. Similarly, CIQ potentiated the function of the GluN2C/2D subunit of the NMDA receptor in WT mice but potentiated only the GluN2C subunit in GluN2D KO mice. The potentiation of both the GluN2C and GluN2D subunits did not induce motor impairment in WT mice but induced motor impairment in GluN2D KO mice. Based on the balance between two competing forces, goal-directed movements could be appropriately performed. Figure is modified from [16]. Red arrows indicate excitatory pathways; gray arrows indicate inhibitory pathways. BS/SC, brain stem/spinal cord; CBC, cerebellar cortex; CM, centromedian nucleus of the thalamus; DCN, deep cerebellar nuclei; GPe, globus pallidus external segment; GPi, globus pallidus internal segment; Pf, parafascicular nucleus of the thalamus; PN, pontine nucleus; PPN, pedunculopontine nucleus; SNr, substantia nigra pars reticulate; SNc, substantia nigra pars compacta; Sth, subthalamic nucleus; VA, ventral anterior nucleus of the thalamus; Vim, ventral intermediate nucleus of the thalamus; VL, ventrolateral nucleus of the thalamus.