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The adenosine A_2A receptor of the basal ganglia

P. J. Richardson

It is widely recognised that Parkinson's disease (PD) is caused by the deterioration of the dopaminergic neurones of the nigrostriatal pathway, resulting in abnormal neural processing in the basal ganglia and consequent motor abnormalities. The current mainstay of therapy for this disease is dopamine replacement using the precursor L-DOPA. However, the duration of L-DOPA therapy is severely limited, and it is associated with the development of incapacitating side-effects such as dyskinesias, on/off episodes and hallucinations. It was therefore of considerable interest when two groups in the late 1980s and early 1990s suggested that the adenosine A_2A receptor could be a suitable target for novel anti-PD drugs. It was hoped that such agents would exhibit fewer side-effects than the current dopamine-based therapies. Indeed it appears that in primate and rodent models of PD, A_2A receptor antagonists do not cause dyskinesias, unlike L-DOPA (Kanda et al. 2000).