Pain is considered one of the most frequent non-motor symptoms of Parkinson’s disease (PD) and it usually manifests before the motor symptoms. Although not considered one of the cardinal symptoms of PD, pain affects up to 80% of PD patients and half of them report multiple types of pain. The cause of this pain is still unknown, but it may be due to dysfunction of key nuclei in the processing of nociceptive information.In order to determine the possible causes of this prodromal symptom, we use different parkinsonian models, such as the hα- syn1-120 model, which presents a differential expression of truncated human α-synuclein under the promoter of the TH, or the Aphakia model, a transgenic mouse model with absence of Pitx3 -/-.Using a battery of behavioral tests to determine the pain threshold, we found that the aphakia and the hα-syn1-120 models show an increased pain sensitivity when subjected to mechanical, thermal and allodynia pain tests compared to wild type mice.These results demonstrate that both PD models represent an ideal tool to unmask the implication of dopamine and noradrenaline neurons in the pain sensitivity signs associated with PD, and to study specific PD-related degeneration, mechanisms and microcircuit dysfunctions directly linked to pain sensitivity in an effort to provide new and more advanced mechanism-based therapies for a better control of pain in PD.