Neurochemical Compensation After Nigrostriatal Bundle Injury in an Animal Model of Preclinical Parkinsonism

doi:10.1001/archneur.1984.04050190062015

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Vol. 41 No. 8, August 1984

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Neurochemical Compensation After Nigrostriatal Bundle Injury in an Animal Model of Preclinical Parkinsonism

Michael J. Zigmond, PhD; Ann L. Acheson, PhD; Michal K. Stachowiak, PhD; Edward M. Strickerm, PhD

Arch Neurol. 1984;41(8):856-861.

Abstract

• Parkinson's disease usually involves a lengthy preclinicalperiod during which few neurological symptoms are observed despiteextensive damage to the dopaminergic nigrostriatal bundle. Injuryto this projection in the rat also fails to produce major neurologicaldysfunctions. In our studies, damage to the nigrostriatal bundleof the rat, resulting in the loss of up to 95% of the dopaminergicterminals in striatum, was accompanied by apparent increasesin the synthesis and release of dopamine (DA) from those dopaminergicterminals that remained. More specifically, both the activityof the rate-limiting biosynthetic enzyme, tyrosine hydroxylase,and the content of the principal DA metabolite, dihydroxyphenylaceticacid, were increased in striatum relative to DA levels. Theincreases were exponentially related to DA loss.

Author Affiliations

From the Departments of Biological Sciences, Psychology, and Psychiatry, University of Pittsburgh. Dr Acheson is now at the Max-Plank-Institut for Psychiatry, Munich.

Footnotes

Accepted for publication Oct 13, 1983.

Reprint requests to 573 Crawford Hall, Department of BiologicalSciences, University of Pittsburgh, Pittsburgh, PA 15260 (DrZigmond).

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