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NEUROLOGY 1975;25:483
© 1975 American Academy of Neurology

Brain H3-catecholamine metabolism in experimental cerebral ischemia

MICHAEL H. LAVYNE, M.D., MICHAEL A. MOSKOWITZ, M.D., FRANCES LARIN, B.S., NICHOLAS T. ZERVAS, M.D. and RICHARD J. WURTMAN, M.D.

Laboratory of Neuroendocrine Regulation, Department of Nutrition and Food Science, Massachusetts Institute of Technology, Cambridge, and the Department of Neurosurgery, Beth Israel Hospital, Harvard Medical School, Boston (Dr. Zervas).

Unilateral ligation of a common carotid artery in gerbils causes a major depletion of brain dopamine, which is most marked in brain regions known to receive dopaminergic projections. To determine whether this depletion reflects release of stored dopamine, a radioactive label (H3-dopamine) was introduced into brain dopamine pools 4 hours prior to ligation. Twenty-four hours later, brain H3-catecholamines were profoundly depressed ipsilateral to the lesion among animals exhibiting clinical signs of stroke. Within brain regions known to receive dopaminergic projections, common carotid ligation also was associated with a selective decrease in the concentration of H3-deaminated metabolites. These data suggest that cerebral ischemia is associated with release of catecholamines, as well as with impaired oxidative metabolism of catecholamines.

These studies were supported in part by USPHS grants NS-10459, HL15365, and GM-2019.

Received for publication September 9, 1974.

Dr. Lavyne's address is Department of Nutrition and Food Science, Laboratory of Neuroendocrine Regulation, Massachusetts Institute of Technology, Cambridge, MA 02139.




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