Depletion of unilateral striatal dopamine impairs initiation of contralateral actions and not sensory attention.
Although Parkinson's disease has traditionally been considered as a motor disorder, there has been much recent interest in the nature and the neural substrates of parkinsonian dementia and cognitive dysfunction. These disabilities, which can induce visuospatial impairment and visual 'neglect', may also have a bearing on the controversy about the normal functions of the nigrostriatal dopamine (DA) projection and the basal ganglia. The observations that neurones in both substantia nigra and striatum respond to sensory events in terms of neuronal firing or DA release, also suggest a role for striatum in sensorimotor integration. An important behavioural correlate of this integration is the 'sensorimotor neglect' syndrome in animals with unilateral lesions of the nigrostriatal projection who fail to orient to contralateral sensory events. However, this neglect may arise not from contralateral sensory inattention, but from an inability to express this sensory selection via motor output. We present here two lines of evidence that unilateral striatal DA depletion in the rat does not affect sensory attention to visual signals of reward, but rather impairs the initiation (though not the completion) of contralateral motor acts. These results not only help to clarify the function of the nigrostriatal DA projection, but also show that depletion in this system is linked specifically to a process of response initiation, which may be the fundamental impairment in Parkinson's disease.
D000818:Animals; D003342:Corpus Striatum / Q000502:physiology*; D004195:Disease Models, Animal; D004298:Dopamine / Q000502:physiology*; D007839:Functional Laterality; D006892:Hydroxydopamines / Q000633:toxicity; D008297:Male; D009068:Movement; D010300:Parkinson Disease / Q000503:physiopathology*; D051381:Rats; D013378:Substantia Nigra / Q000502:physiology*
D006892:Hydroxydopamines; D004298:Dopamine