The ability to accurately determine when to perform actions is a fundamental function of the nervous system and vital to shaping behavioral responses that achieve there intended outcome. Fixed-interval reinforcement schedules require animals to respond following a specified interval duration in order to obtain a reward. When reinforcement trials are interleaved with non-rewarded, or probe, trials during training, animals develop peak press distributions in these omission trials around the reinforced time. This peak press distribution under omission conditions indicates animals can correctly start and stop responding in a manner according to when the reward outcome would be expected. The cortex and striatum have been canonically implicated in action timing and behavioral models have proposed the idea that action behavioral states during motor timing performance could play a role in the pacing of action with respect to time. In this dissertation, I describe a sensorimotor feedback mechanism in which modal cortical activation by action-derived sensory cues is utilized to shape response dynamics in a self-paced fixed-interval timing task. Acute deprivation of the action-cued sensory modality, but not other action-based senses, is sufficient to disrupt timing dynamics in trained animals. Staining for immediate early gene protein expression in animals that performed the motor timing task revealed active populations in a modal cortical region related to pressing. Using an activity-dependent labeling system that exploits the cFos promoter, action-triggered optical activation of these populations via channelrhodopsin, partially rescues the key features of learned action timing behavior under sensory deprivation. Finally, using a viral activity-dependent labeling strategy in combination with the retrograde adeno-associated virus serotype, I demonstrate a role of layer V, striatal-projecting populations in task performance also under a sensory deprived state. These data point toward a feedback component of motor timing control in which modal cortices and the basal ganglia transduce self-generated sensory cues to assist in performing complex motor timing patterns.