Abstract
Adenosine A2A receptors are highly expressed in caudate-putamen, and external globus pallidus (GPe), but in trace in internal globus pallidus/entopeduncular nucleus. A2A upregulation in striatal-pallidal pathway is associated with levodopa dyskinesias in Parkinson's disease. Instead, A2A downregulation has been reported in striatum of Huntington Disease. We investigated distribution of A2A receptors in basal ganglia of Tor1a+/− knock-out mouse model DYT1 primary dystonia.
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