Ecstasy counteracts catalepsy in rats, an anti-parkinsonian effect?

Parkinson's disease is due to a dopamine deficiency caused by the degeneration of midbrain dopamine neurons. Current therapies are aimed to substitute dopamine or to directly stimulate postsynaptic dopamine receptors. However, not all patients profit from current therapies to the same extent, e...

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Bibliographic Details
Published in:Neuroscience letters 2002-09, Vol.330 (3), p.251-254
Main Authors: Schmidt, Werner J., Mayerhofer, Andreas, Meyer, Anja, Kovar, Karl-A.
Format: Article
Language:English
Subjects:
3,4-Methylenedioxyamphetamine
3,4-Methylenedioxyamphetamine - analogs & derivatives
3,4-Methylenedioxyamphetamine - pharmacology
3,4-Methylenedioxyethylamphetamine
3,4-Methylenedioxymethamphetamine
Adrenergic Uptake Inhibitors - pharmacology
Animals
Biological and medical sciences
Catalepsy
Catalepsy - chemically induced
Catalepsy - drug therapy
Catalepsy - physiopathology
Dopamine Antagonists - pharmacology
Dose-Response Relationship, Drug
Drug addictions
Ecstasy
Enantiomers
Haloperidol
Haloperidol - pharmacology
Male
Medical sciences
N-Methyl-1-(1,3-benzodioxol-5-yl)-2-butanamine
N-Methyl-3,4-methylenedioxyamphetamine - pharmacology
Parkinson Disease, Secondary - chemically induced
Parkinson Disease, Secondary - drug therapy
Parkinson Disease, Secondary - physiopathology
Parkinson's disease
Rats
Rats, Sprague-Dawley
Toxicology
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Summary:Parkinson's disease is due to a dopamine deficiency caused by the degeneration of midbrain dopamine neurons. Current therapies are aimed to substitute dopamine or to directly stimulate postsynaptic dopamine receptors. However, not all patients profit from current therapies to the same extent, even serious side effects such as dyskinesias are complicating the therapy. Therefore, there is still a need for better anti-parkinsonian drugs. Here we show that some compounds from the ‘Ecstasy’-derivatives exert potent anti-parkinsonian activity. 3,4-Methylenedioxymethamphetamine, ‘Ecstasy’ dose-dependently and very potently reversed haloperidol-induced parkinsonism in the rat. From the supraadditive effect of the enantiomers it may be concluded that both enantiomers contribute to the antiparkinsonian effects at two different target sites.
ISSN:0304-3940
1872-7972
DOI:10.1016/S0304-3940(02)00823-6