Chapter title |
Amphetamine-metabolites of deprenyl involved in protection against neurotoxicity induced by MPTP and 2'-methyl-MPTP.
|
---|---|
Chapter number | 27 |
Book title |
Amine Oxidases: Function and Dysfunction
|
Published in |
Journal of neural transmission Supplementum, January 1994
|
DOI | 10.1007/978-3-7091-9324-2_27 |
Pubmed ID | |
Book ISBNs |
978-3-21-182521-1, 978-3-70-919324-2
|
Authors |
I. Sziráki, V. Kardos, M. Patthy, M. Pátfalusi, J. Gaál, M. Solti, E. Kollár, J. Singer, Sziráki, I., Kardos, V., Patthy, M., Pátfalusi, M., Gaál, J., Solti, M., Kollár, E., Singer, J. |
Abstract |
The ability of 1-deprenyl to protect against the parkinsonian effects of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) has been attributed to the inhibition of conversion of MPTP to MPP+ (1-methyl-4-phenylpyridinium) catalyzed by MAO-B. We report here that deprenyl-treatment in mice has an additional neuroprotective element associated with the rapid metabolization of 1-deprenyl to 1-methamphetamine and 1-amphetamine. 1-Methamphetamine and 1-amphetamine inhibit MPP(+)-uptake into striatal synaptosomes prepared from rats. Post-treatment by 1-deprenyl, 1-methamphetamine, 1-amphetamine (at times when MPTP is no longer present in the striatum of mice) protects against neurotoxicity in C57BL mice by blocking the uptake of MPP+ into dopaminergic neurons, and even against the neurotoxicity induced by 2'CH3-MPTP, which is partly bioactivated by MAO-A. These findings may have clinical implications since deprenyl has recently been found to delay the progression of Parkinson's disease. |
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Demographic breakdown
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Other | 1 | 10% |
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Neuroscience | 1 | 10% |
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