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Brain, Vol. 126, No. 2, 312-325, February 2003
© 2003 Guarantors of Brain
doi: 10.1093/brain/awg035

Dopamine release during sequential finger movements in health and Parkinson’s disease: a PET study

Ines K. Goerendt1, Cristina Messa1,3,4,5, Andrew D. Lawrence1,2, Paul M. Grasby1, Paola Piccini1 and David J. Brooks1

1 MRC Clinical Sciences Centre and Division of Neuroscience, Faculty of Medicine, Imperial College, Hammersmith Hospital, London, 2 MRC Cognition and Brain Sciences Unit, Cambridge, UK, 3 INB-CNR, 4 University of Milano Bicocca and 5 S. Raffaele Institute Milano, Italy. Corresponding author: Andrew Lawrence, MRC Cognition and Brain Sciences Unit, 15 Chaucer Road, Cambridge CB2 2EF, UK E-mail: andrew.lawrence{at}mrc-cbu.cam.ac.uk

Parkinson’s disease is associated with slowness, especially of sequential movements, and is characterized pathologically by degeneration of dopaminergic neurons, particularly targeting nigrostriatal projections. In turn, nigrostriatal dopamine has been suggested to be critical for the execution of sequential movements. The objective of this study was to investigate in vivo, with [11C]raclopride, PET changes in regional brain levels of dopamine in healthy volunteers and Parkinson’s disease patients during the execution of paced, stereotyped sequential finger movements. Striatal [11C]raclopride binding reflects dopamine D2 receptor availability and is influenced by synaptic levels of endogenous dopamine. During execution of a pre-learned sequence of finger movements, a significant reduction in binding potential (BP) of [11C]raclopride was seen in both caudate and putamen in healthy volunteers compared with a resting baseline, consistent with release of endogenous dopamine. Parkinson’s disease patients also showed attenuated [11C]raclopride BP reductions during the same motor paradigm in striatal areas less affected by the disease process. These findings confirm that striatal dopamine release is a component of movement sequencing and show that dopamine release can be detected in early Parkinson’s disease during a behavioural manipulation.


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