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J Neurophysiol 84: 549-557, 2000;
0022-3077/00 $5.00
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The Journal of Neurophysiology Vol. 84 No. 1 July 2000, pp. 549-557
Copyright ©2000 by the American Physiological Society

Dopamine D1 Agonist Activates Temporal Lobe Structures in Primates

Kevin J. Black,1,2,3,5 Tamara Hershey,1 Mokhtar H. Gado,2,3,5 and Joel S. Perlmutter2,3,4,5

Departments of  1Psychiatry,  2Neurology and Neurological Surgery,  3Radiology, and  4Anatomy and Neurobiology, Washington University School of Medicine; and  5The Mallinckrodt Institute of Radiology, St. Louis, Missouri 63110

Black, Kevin J., Tamara Hershey, Mokhtar H. Gado, and Joel S. Perlmutter. Dopamine D1 Agonist Activates Temporal Lobe Structures in Primates. J. Neurophysiol. 84: 549-557, 2000. Changes in the function of dopamine D1-influenced neuronal pathways may be important to the pathophysiology of several human diseases. We recently developed methods for averaging functional imaging data across nonhuman primate subjects; in this study, we apply this method for the first time to map brain responses to experimental dopamine agonists in vivo. Here we report the use of positron emission tomography (PET) in seven normal baboons to measure the regional cerebral blood flow (rCBF) responses produced by an acute dose of the dopamine D1 full agonist SKF82958. The most significant rCBF increases were in bilateral temporal lobe, including amygdala and superior temporal sulcus (6-17%, P < 0.001). Blood flow decreased in thalamus, pallidum, and pons (4-7%, P = 0.001). Furthermore the rCBF responses were dose-dependent and had a half-life of ~30 min, similar to that reported for the drug's antiparkinsonian effects. Absolute whole-brain blood flow did not change, suggesting that these local changes in rCBF reflect neuronal rather than direct vascular effects of the agonist. The prominent temporal lobe response to a D1 agonist supports and extends our recent observations that levodopa produces prominent amygdala activation both in humans and in other primates. We speculate that levodopa may exert its known effects on mood in humans through increased amygdala activity, mediated in part by D1 receptors.




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