Molecular neuroanatomic mechanisms of Parkinson's disease: a proposed therapeutic approach.

Current concepts suggest that parkinsonian bradykinesia is a consequence of an imbalance between striatopallidal and striatonigral output pathways. Dopamine appears to oppositely effect these neurons due to the selective localization of the D1 receptor on striatonigral neurons and the D2 receptor on striatopallidal neurons. Studies measuring changes in gene regulation suggest how selective D1 and D2 dopamine agonist treatments may be used to restore the normal balance between the striatal output pathways.