No Evidence Of Sensory Neuropathy In A Traditional Mouse Model Of Idiopathic Parkinson’s Disease

Parkinson’s disease (PD) is the second-most common neurodegenerative disorder worldwide and is diagnosed based upon motor impairments. Non-motor symptoms are well-recognized in PD, and peripheral neuropathy is a frequent but poorly appreciated non-motor sign. Study of how the central and peripheral sensory systems are affected can contribute to the development of targeted therapies and deepen the understanding of the pathophysiology of PD. Although the cause of sporadic PD is unknown, chronic exposure to the pesticide rotenone in humans increases the risk of development of PD. Here, we aimed to investigate whether peripheral neuropathy is present in a traditional model of PD. Mice receiving intrastriatal rotenone showed greatly reduced dopamine terminals in the striatum and reduction in tyrosine hydroxylase-positive neurons in the Substantia nigra pars compacta and developed progressive motor impairments in hindlimb stepping and rotarod but no change in spontaneous activity. Interestingly, repeated testing using gold-standard protocols showed no change in gut motility, a well-known non-motor symptom of PD. Importantly, we did not observe any change in heat, cold, or touch sensitivity, again based upon repeated testing with well-validated protocols that were statistically well-powered. Therefore, this traditional model fails to replicate PD, and our data again reiterate the importance of the periphery to the disorder that is PD.