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Role of dopamine in ischemic striatal injury

Metabolic evidence

Department of Neurology (Drs. Globus and Ginsberg, Mr. Busto, and Dr. Dietrich), Cerebral Vascular Research Center, University of Miami School of Medicine, Miami, FL, and the Department of Neurology (Dr. Harik), University Hospitals of Cleveland and Case Western Reserve University School of Medicine, Cleveland, OH.

We studied the effect of a prior unilateral substantia nigra lesion on the recovery of local cerebral glucose utilization (ICMRgl) and blood flow (ICBF), measured autoradiographically, following 30 minutes of forebrain ischemia in rats. On the lesioned side, striatal dopamine (DA) and its metabolites were depleted by more than 95% and did not change after ischemia. In contrast, significant increases in striatal DA metabolites occurred on the nonlesioned side following ischemia. Despite unilateral DA depletion, no side-to-side ICBF differences were observed. However, the normally occurring postischemic restoration of ICMRgl in the dorsolateral striatum at 2 and 4 hours of recirculation was suppressed on the DA-depleted side, and the degree of ICMRgl/ICBF uncoupling diminished. These results suggest that integrity of the DA system accentuates postischemic metabolism/flow uncoupling in the striatum and may therefore contribute to selective ischemic injury of this structure.

Address correspondence and reprint requests to Dr. Globus, Department of Neurology (D4-5), University of Miami School of Medicine, PO Box 016960, Miami, FL 33101.

Supported by USPHS grants NS-05820, NS-22603, and NS-18150, and by Grant-in-Aid 85–1258 of the American Heart Association, with funds contributed in part by the Greater Miami Chapter. Dr. Ginsberg is the recipient of a Jacob Javits Neuroscience Investigator Award. Dr. Dietrich is an Established Investigator of the American Heart Association.

Received December 1, 1586. Accepted for publication in final form January 21, 1587.

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