The primary motor cortex (M1) is crucial for movement execution, especially dexterous ones, but also for cognitive functions like motor learning. The acquisition of motor skills to execute dexterous movements requires dopamine-dependent and -independent plasticity mechanisms within M1. In addition to the basal ganglia, M1 is disturbed in Parkinson’s disease (PD). However, little is known about how the lack of dopamine (DA), characteristic of PD, directly or indirectly impacts M1 circuitry. Here we review data from studies of PD patients and the substantial research in non-human primate and rodent models of DA depletion. These models enable us to understand the importance of DA in M1 physiology at the behavioral, network, cellular, and synaptic levels. We first summarize M1 functions and neuronal populations in mammals. We then look at the origin of M1 DA and the cellular location of its receptors and explore the impact of DA loss on M1 physiology, motor, and executive functions. Finally, we discuss how PD treatments impact M1 functions.