Parkinson’s disease (PD) is a neurological and neurodegenerative disease characterized by themanifestation of motor and non-motor symptoms. Among these, pain is one of the most frequent,affecting around 85% of patients and contributing to a deterioration in their quality of life.Nowadays, pain treatment in PD is still inefficient due to the lack of knowledge of the underlyingmechanisms. However, we know that pain can be modulated by the monoaminergic descendingpathways projecting to the dorsal horn of the spinal cord (DHSC). Thus, the aim of the present studyis to unravel the involvement of the hypothalamic A11 nucleus, considered as the main source ofdopamine in the DHSC, in the control of the nociceptive impairments in 6-OHDA mouse model of PD.After characterizing the anatomical, behavioral and electrophysiological abnormalities in this model,we used optogenetic approaches to selectively modulate the A11 dopaminergic neurons projectingto the lumbar DHSC. We first demonstrated that the activation of A11 dopaminergic descendingpathway is able to improve mechanical allodynia in 6-OHDA mice without affecting motor disabilities.Furthermore, we also show that this activation may have an effect on nociceptive integration in thewide dynamic range neurons of the DHSC. These results highlight the crucial role of nucleus A11 inthe pathophysiology of pain caused by damage to dopaminergic neurons in the substantia nigra, andsuggest a new therapeutic pathway involving this nucleus in the treatment of pain in Parkinson'sdisease.