Brain activity in the beta frequency range (~12–30 Hz) in motor cortex (MC) and subthalamic nucleus (STN) is related to motor behavior. Because MC β-power is pathologically elevated in parkinsonian states, it has been identified as a putative biomarker of symptom severity and considered a potential control signal for closed-loop/smart deep brain stimulation (DBS). In recent experimental work, we targeted DBS to the STN of parkinsonian rodents while collecting neural field potentials. During high frequency (150–250 Hz) stimulation, mean MC β-power was suppressed whether or not the treatment alleviated symptoms, but variations about that mean changed with DBS efficacy. In asymptomatic rats, MC β-power was strongly anticorrelated with gait speed; in parkinsonian rats, including those being treated unsuccessfully, MC β-power was independent of gait speed. Thus, the magnitude of MC β-power is less relevant than it having a strong relationship to movement intensity, and effective DBS restores that relationship. 

With the role of β-power unclear, several groups are instead focusing on β-coherence between MC and STN. We report that during low intensity movements, alterations in MC-STN β-coherence are small and unrelated to behavior. However, in healthy rodents during self-directed behavior reversals — e.g., quick stop followed by rapid acceleration — MC-STN β-coherence is prominently elevated. In contrast, parkinsonian rodents performing self-directed behaviors exhibit suppressed MC-STN β-coherence. These results suggest that in healthy animals, intense motor activity is mediated partly via strong β-frequency signaling from STN to MC; in parkinsonian animals, the β-frequency signals in STN are aberrant, and motor activity is enabled by their suppression.