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© 1995 Oxford University Press

research-article

Central Nervous System Toxicity of Manganese

I. Inhibition of Spontaneous Motor Activity in Rats after Intrathecal Administration of Manganese Chloride

RUSSELL T. INGERSOLL*, ERWIN B. MONTGOMERY, JR.{dagger} and H. VASKEN APOSHIAN{ddagger},§,1,2

*Department of Pharmacology and Toxicology, College of Pharmacy, University of Arizona Tucson, Arizona 85724 {dagger}Department of Neurology, University of Arizona Tucson, Arizona 85724 {ddagger}Department of Pharmacology. College of Medicine, University of Arizona Tucson, Arizona 85724 §University Department of Molecular and Cellular Biology, Life Sciences South 444, Faculty of Science, University of Arizona Tucson, Arizona 85721

Received June 13, 1994; accepted January 31, 1995

The intrathecal administration of MnCl2 to young male rats caused doparnine depletion in the caudate-putamen and a decrease in spontaneous motor activity. Our experiments demonstrate that in the young rat: (a) the lateral choroid plexus protects the cerebrospinal fluid (CSF) from high concentrations of Mn in the blood by sequestering and thus preventing large amounts of this metal ion from entering the CSF. As blood Mn levels rise, the lateral choroid plexus may become overwhelmed and leak an increasing amount of Mn into the CSF. (b) The lateral choroid plexus does not remove Mn2+ from the CSF. (c) The injection of MnCl2 into the CSF of rats caused a rapid decrease in spontaneous motor activity which is dose-dependent and reversible under the present experimental conditions. Entrathecal Mn results in a substantial decrease in striatal dopamine but not homovanillic acid or 3,4-dihydroxyphenylacetic acid (DOPAC) concentrations and is associated with an increase in the Mn concentration of the substantia nigra and caudate-putamen.


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