Parkinson’s disease (PD) is a progressive disorder of the nervous system, affecting 1% of the ageing population. Common motor symptoms include tremor and bradykinesia, while non-motor symptoms range from constipation to sleep disturbances. The neuropathological hallmarks involve the loss of dopaminergic neurons in the substantia nigra and abnormal intra-neuronal accumulation of Lewy bodies. Here, the zebrafish model is used to investigate the behavioural defects associated with PD. Mutations of PARK2, PINK1, PARK7, LRRK2 and SNCA genes cause different forms of PD in humans. Using CRISPR/Cas9 gene editing, we generate knockout models of these PD-associated genes in zebrafish. While the zebrafish models exhibit a loss of certain diencephalic populations of dopaminergic neurons, this does not result in clear symptoms. Thus, we use high-throughput behavioural assays with high spatio-temporal resolution to characterise fast escape responses and slower exploratory swimming. Certain of the models exhibit a long-latency response, with reduced tail kinematics, in response to acoustovestibular stimuli. During exploration, PINK1 and SNCA models exhibit lower swimming activity. Additionally, a tendency to perform more turns than forward swims is observed, correlating with the impact of disease on motor control. The analysis of locomotor phenotypes is extended at juvenile stages, where all models exhibit reduced swimming activity, correlating with the bradykinesia observed in patients. Finally, we explore sleep defects to understand the non-motor nature of PD in these models. Ultimately, building a phenotypic profile could enable zebrafish to facilitate and accelerate the progress of screening for new therapeutic targets and candidate chemicals for PD.