Movement Disorders (revue)

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Dopaminergic innervation of the human striatum in Parkinson's disease

Identifieur interne : 000B53 ( Istex/Curation ); précédent : 000B52; suivant : 000B54

Dopaminergic innervation of the human striatum in Parkinson's disease

Auteurs : Michelle Porritt [Australie] ; Davor Stanic [Australie] ; David Finkelstein [Australie] ; Peter Batchelor [Australie] ; Sharon Lockhart [Australie] ; Andrew Hughes [Australie] ; Renate Kalnins [Australie] ; David Howells [Australie]

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RBID : ISTEX:35F93298749899476065692D8C2CD520C41A46C2

English descriptors

Abstract

In Parkinson's disease (PD), dopaminergic input to the caudate nucleus and a band of putaminal tissue abutting the external globus pallidus seems well preserved on immunohistochemical staining for the dopamine transporter. Counting of dopaminergic terminals showed that terminal density in these regions in PD was the same as that in controls, which indicates that input is truly preserved and not a consequence of a compensatory upregulation of metabolism in a reduced pool of surviving terminals. When the branching pattern of dopaminergic axons coursing through the globus pallidus was examined, we found no evidence for increased axonal sprouting in PD that might have contributed to preservation of dopaminergic input to the putamen or caudate nucleus. Although terminal counting indicated that anatomic input was preserved to parts of the striatum, dopamine uptake site density in these regions was reduced significantly. This suggests that the impact of disease in these areas is more profound than was thought previously. © 2005 Movement Disorder Society

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DOI: 10.1002/mds.20399

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ISTEX:35F93298749899476065692D8C2CD520C41A46C2

Le document en format XML

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<div type="abstract" xml:lang="en">In Parkinson's disease (PD), dopaminergic input to the caudate nucleus and a band of putaminal tissue abutting the external globus pallidus seems well preserved on immunohistochemical staining for the dopamine transporter. Counting of dopaminergic terminals showed that terminal density in these regions in PD was the same as that in controls, which indicates that input is truly preserved and not a consequence of a compensatory upregulation of metabolism in a reduced pool of surviving terminals. When the branching pattern of dopaminergic axons coursing through the globus pallidus was examined, we found no evidence for increased axonal sprouting in PD that might have contributed to preservation of dopaminergic input to the putamen or caudate nucleus. Although terminal counting indicated that anatomic input was preserved to parts of the striatum, dopamine uptake site density in these regions was reduced significantly. This suggests that the impact of disease in these areas is more profound than was thought previously. © 2005 Movement Disorder Society</div>
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