Skip Navigation LinksHome > September 2010 - Volume 69 - Issue 9 > Hyperdopaminergic Status in Experimental Huntington Disease
Journal of Neuropathology & Experimental Neurology:
doi: 10.1097/NEN.0b013e3181ee005d
Original Articles

Hyperdopaminergic Status in Experimental Huntington Disease

Jahanshahi, Ali MSc; Vlamings, Rinske MSc; Kaya, Ahmet Hilmi MD; Lim, Lee Wei MD, PhD; Janssen, Marcus L.F. MD; Tan, Sonny MD; Visser-Vandewalle, Veerle MD, PhD; Steinbusch, Harry W.M. PhD; Temel, Yasin MD, PhD

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Abstract

Huntington disease has been linked to increased dopaminergic neurotransmission in the striatum, and clinical studies have demonstrated that the associated chorea can be treated with dopamine antagonist or dopamine-depleting drugs. The origin of this hyperdopaminergic status is unknown. Because substantia nigra pars compacta and the ventral tegmental area are the main sources of striatal dopamine input, we hypothesized that changes in these regions relate to striatal dopaminergic alterations. Here, in a recently generated transgenic rat Huntington disease model that shows progressive striatal neurodegeneration and chorea, we found evidence ofincreased dopamine levels in the striatum. We also demonstrate more dopaminergic cells in the substantia nigra pars compacta and ventral tegmental area in these rats. These results suggest that increased striatal dopamine comes from these 2 main nuclei, and that it is not necessarily related to shrinkage of the striatum. The findings implicate increased dopamine input from these nuclei in the pathogenesis of chorea in Huntington disease.

© 2010 American Association of Neuropathologists, Inc

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