Intraoperative human brain recordings during a memory task reveal that when participants inhibit memory formation, the subthalamic nucleus shows higher beta power and beta coherence with areas of the lateral cortex implicated in memory processing.
Activation of the subthalamic nucleus (STN) pauses or disrupts behavior, while STN inhibition reduces the disruptive effects of surprise, indicating that STN activation is both sufficient and necessary for behavioral inhibition.
In mouse models of Huntington's disease, the subthalamic nucleus, which suppresses movements, also exhibits impaired glutamate homeostasis, NMDA receptor-dependent mitochondrial oxidant stress, firing disruption, and 30% neuronal loss.
When coupling between STN spikes and cortical gamma oscillations was strong, subsequent movement was initiated earlier, independent of changes in mean firing rates, demonstrating the importance of relative spike timing.
Patterns of coordinated activity in the basal ganglia predict how much force we will use to grip objects, suggesting that individuals with paralysis may ultimately be able to use these signals to control graded responses in robotic devices.