Volume 939, Issue 1 p. 330-339

Rescue of Dying Neurons by (R)-Deprenyl in the MPTP-Mouse Model of Parkinson's Disease Does Not Include Restoration of Neostriatal Dopamine

STEFANUS J. STEYN

STEFANUS J. STEYN

Harvey W. Peters Center for the Study of Parkinson's Disease, Department of Chemistry, Virginia Tech., Blacksburg, Virginia, U.S.A.

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KAY CASTAGNOLI

KAY CASTAGNOLI

Harvey W. Peters Center for the Study of Parkinson's Disease, Department of Chemistry, Virginia Tech., Blacksburg, Virginia, U.S.A.

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NEAL CASTAGNOLI JR.

Corresponding Author

NEAL CASTAGNOLI JR.

Harvey W. Peters Center for the Study of Parkinson's Disease, Department of Chemistry, Virginia Tech., Blacksburg, Virginia, U.S.A.

Address for correspondence: Neal Castagnoli, Jr., Ph.D. Harvey W. Peters Center Department of Chemistry, Virginia Tech., Blacksburg, VA 24061-0212, U.S.A. Voice: 540-231-8200; fax: 540-231-8890; [email protected].Search for more papers by this author
First published: 25 January 2006
Citations: 1

Abstract

Abstract: Chronic (8- to 10-week) administration of the selective, potent, and irreversible monoamine oxidase B inhibitor (R)-deprenyl has been shown to increase the tyrosine hydroxylase immunoreactivity in the substantia nigra of mice that had been treated three days earlier with a neurotoxic dose of the parkinsonian-inducing agent 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). This reported rescuing of lesioned nigrostriatal cell bodies by (R)-deprenyl prompted us to investigate if this (R)-deprenyl treatment also could restore neostriatal dopamine levels that are depleted by MPTP. The results of these experiments show that long term (8 or 10 weeks) treatment with (R)-deprenyl beginning three days post MPTP administration did not result in restoration of depleted neostriatal dopamine levels in C57BL/6 mice. We conclude that, although (R)-deprenyl may rescue MPTP-injured nigrostriatal neurons, it does not lead to functional recovery of these neurons as measured by the restoration of neostriatal dopamine levels.