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Subthalamic nucleus and striatum: The red and green signals to regulate the traffic of basal ganglia circuitry

The “race model” of basal ganglia (BG) circuits function concurrently to achieve the balance between the “go” pathways mediated by striatonigral projections and the “stop” pathways mediated by the STN/substantia nigra pars reticulata (SNr). The final outcome depends on the modulatory effects of these two pathways on the output structure (SNr). Despite many studies that have explored this mutual response inhibition model using “stop-signal” reaction time paradigms, the exact nature of the function in the different BG structures, and the fine timing between these activities, remains elusive. The recent study by Schmidt et al. investigated this idea with their elegant study in normal rats trained in the stopsignal task. They used microelectrode tetrads to quantify the neuronal activities in various BG structures (striatum, STN, SNr, and globus pallidus) of freely behaving animals responding to go and stop signals provided by visual and auditory cues by entering into different apertures in their cage and collecting food pellets for successful trials. The outcome was a transient increased activity of the STN (approximately 15 ms after the stop cue) for both failed and correct stop cues, which promptly conveyed on to the SNr (approximately 13 ms after STN peak activity). However, the go signal mediated by striatonigral pathways were already initiated (the stop cue was presented approximately 50 ms before movement onset), the gamma-aminobutyric acid– mediated striatal signals overrode the glutamatergic STN stimulation and finally disinhibited BG output, resulting in movement. Thus, the green go signal of striatum and red stop signal of the STN maintains the traffic of BG circuits by inhibiting or activating the final motor output, depending on the timing of presentation of sensory cue to these structures. Although this concept of the race model is not new, this study, with fine timing between the peak activities of various structures involved in go and stop processes, opens up further interesting questions in this exciting field. How the striatal neuronal activity shuts off in the process of stop has to be validated to account for superior control of the striatum. Furthermore, the role of sensory afferent pathways from the cortex or thalamus needs to be further investigated during movement. Studying the coordination of these two pathways in disease models affecting basal ganglia disorders also needs to be performed. Nevertheless, this new idea and findings open up new ways of looking at basal ganglia physiology.