Dopamine (DA) is classically associated with learning and reward prediction error, though it is clear from deficits in the striatal dopaminergic system that DA plays a major, yet unclear, role in controlling motor behaviour. Several recent works have begun to uncover the complex roles DA plays in movement control. We have developed an experimental framework based on a dual fibre-photometry system, EMG recording and a freewheeling linear treadmill to explore the dynamics of dLight readouts during spontaneous locomotion and brief muscle twitches in head-fixed mice. In this work, we find high correlations between the striatal DA signalling in both hemispheres. We show distinct transient decreases in the DA signal before initiation of locomotion, as well as increases in the signal after termination of locomotion. During postural shifts, we observed a characteristic tri-phasic signal, closely matching the signal predicted from the firing pattern of midbrain dopaminergic cells in earlier work. We also examined how these features of DA signalling are disrupted in two mouse models of Parkinsonism: a model of early Parkinsonism induced by intracerebral injection of pre-formed fibrils of alpha-synuclein, and a model of late Parkinsonism induced by intracerebral injection of the toxin 6-hydroxydopamine, a toxin which promotes dopaminergic cell death. We reveal slowing of the movement-related DA signals, and reduction in the interhemispheric correlation, but with no qualitative changes in the signalling patterns. We conclude that striatal DA signals differ according to the type of movement performed, and that movement-related DA dynamics are altered in Parkinsonism.