Journal
NEUROIMAGE
Volume 20, Issue 2, Pages 1064-1075Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/S1053-8119(03)00348-3
Keywords
positron emission tomography; volume rendering; MPTP; Parkinson's disease
Funding
- NINDS NIH HHS [NS P50-39793] Funding Source: Medline
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Neurophysiological studies of the brain in normal and Parkinson's disease (PD) patients have indicated intricate connections for basal ganglia-induced control of signaling into the motor cortex. To investigate if similar mechanisms are controlling function in the primate brain (Macaca fascicularis) after MPTP-induced neurotoxicity, we conducted PET studies of cerebral blood flow, oxygen and glucose metabolism, dopamine transporter, and D2 receptor function. Our observations after MPTP-induced dopamine terminal degeneration of the caudate and putamen revealed increased blood flow (15%) in the globus pallidus (GP), while blood flow was moderately decreased (15-25%) in the caudate, putamen, and thalamus and 40 % in the primary motor cortex (PMC). Oxygen extraction fraction was moderately increased (10-20%) in other brain areas but the thalamus, where no change was observable. Oxygen metabolism was increased in the GP and SMA (supplementary motor area including premotor cortex, Fig. 3) by a range of 20-40% and decreased in the putamen and caudate and in the PMC. Glucose metabolism was decreased in the caudate, putamen, thalamus, and PMC (range 35-50%) and enhanced in the GP by 15%. No change was observed in the SMA. In the parkinsonian primate, [C-11]CFT (2beta-carbomethoxy-3beta-(4-fluorophenyltropane) dopamine transporter binding was significantly decreased in the putamen and caudate (range 60-65%). [C-11]Raclopride binding of dopamine D-2 receptors did not show any significant changes. These experimental results obtained in primate studies of striato-thalamocortico circuitry show a similar trend as hypothetized in Parkinson's disease-type degeneration. (C) 2003 Elsevier Inc. All rights reserved.
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