Behavioral analysis of motor and non-motor symptoms in rodent models of Parkinson's disease.

Alongside the classical motor symptoms, non-motor symptoms are increasingly recognised to play a major role in the disability associated with Parkinson's disease in humans. Animal models based on experimental depletion of forebrain dopamine have traditionally focussed on the simple and easy to measure motor impairments, and they reproduce well the bradykinesia, rigidity and impairments in the initiation and sequencing of voluntary goal-directed movement. However, a more comprehensive analysis is now urgently required. In this chapter we summarise the predominant unilateral and bilateral dopamine lesion, toxin and genetic models of human parkinsonism, and review the consequences in more complex cognitive, motor learning and psychiatric ('behavioural') domains. Theoretical and experimental advances in our understanding of information processing and associative plasticity within the striatum are not only revolutionising our understanding of normal striatal function but also bear directly on our understanding of the processes that underlie non-motor as well as motor disability in human disease, including in Parkinson's disease.