Abstract:
:Subthalamic nucleus (STN) hyperactivity follows lesions of mesencephalic dopaminergic neurons in animal models of Parkinson's disease. The mechanism leading to sustained STN hyperactivity in parkinsonism is not well understood, but it seems not to depend on the integrity of striato-pallido-subthalamic connections (the so called indirect pathway). Sustained STN hyperactivity could result from the loss of the direct dopaminergic innervation of the STN. Here we report increased [125I]sulpiride binding in the STN of rats with 6-hydroxydopamine (6-OHDA) lesions of mesencephalic dopaminergic neurons. Furthermore, we found that chronic oral treatment with levodopa reverted the lesion-induced increase in [125I]sulpiride binding. Our results demonstrate that most STN D2-class dopamine receptors are postsynaptic to afferent dopaminergic fibers. Furthermore, they suggest that alterations of local STN dopaminergic mechanisms could play a role in the pathophysiology of parkinsonism and mediate the therapeutic/adverse effects of chronic levodopa administration.
journal_name
Neuroreportjournal_title
Neuroreportauthors
Murer MG,Ferrario J,Delfino M,Dziewczapolski G,Gershanik OS,Raisman-Vozari Rdoi
10.1097/00001756-199905140-00020subject
Has Abstractpub_date
1999-05-14 00:00:00pages
1501-5issue
7eissn
0959-4965issn
1473-558Xjournal_volume
10pub_type
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