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To address this paradox, STN activity was recorded and manipulated in head-fixed mice at rest and during self-initiated and -paced treadmill locomotion. The majority of STN neurons (type 1) exhibited locomotion-dependent increases in activity, with half encoding the locomotor cycle. A minority of neurons exhibited dips in activity or were uncorrelated with movement. Brief optogenetic inhibition of the dorsolateral STN (where type 1 neurons are concentrated) slowed and prematurely terminated locomotion. In Q175 Huntington\u2019s disease mice abnormally brief, low-velocity locomotion was specifically associated with type 1 hypoactivity. 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