A CORTICO-BASAL GANGLIA CIRCUIT WITHHOLDS IMPULSIVE ACTIONS TO ENABLE PROLONGED EVIDENCE EVALUATION

Decisions about changing sensory environments often unfold over seconds, requiring sustained suppression of impulsive actions while evidence is evaluated. How the brain maintains this prolonged action restraint remains unresolved. We identify a cortico-basal ganglia circuit that is causally required for impulse control during visual change detection. We provide evidence that this circuit implements a cortically controlled braking mechanism in basal ganglia that operates in parallel to evidence accumulation.

Head-fixed mice monitored noisy visual drifting gratings for 3-15.5 seconds and were trained to lick when detecting sustained changes in speed. Optogenetic silencing revealed the causal necessity of three nodes for impulse control: posterocentral secondary motor cortex (pcMOs), dorsomedial striatum (DMS) with opposing D1/D2 contributions, and DMS-recipient substantia nigra pars reticulata (SNr) neurons. DMS recordings showed ramping activity preceding licking that emerged earlier on trials with failed impulse control, consistent with a failed braking attempt. pcMOs silencing shifted this ramping toward lick onset and increased impulsive licks, suggesting pcMOs may appropriately time reactive ramping dynamics in DMS.

Reaction times to stimulus speed changes were unaffected by pcMOs or DMS silencing, and removing stimulus noise did not abolish impulsive actions induced by pcMOs silencing. These results suggest this circuit enforces action restraint rather than affecting evidence accumulation.

Together, these findings define a pcMOs→DMS→SNr circuit for suppressing impulsive actions during sustained evaluation of visual evidence, where pcMOs shapes basal ganglia reactive braking dynamics to permit prolonged evidence accumulation.