Journal article
Dopamine Depletion Does Not Protect against Acute 1-Methyl-4-Phenyl-1,2,3,6-Tetrahydropyridine Toxicity In Vivo
The Journal of neuroscience, v 25(41), pp 9428-9433
12 Oct 2005
PMID: 16221852
Featured in Collection : UN Sustainable Development Goals @ Drexel
Abstract
Dopamine (DA) has been postulated to play a role in the loss of dopaminergic substantia nigra (SN) neurons in Parkinson's disease because of its propensity to oxidize and form quinones and other reactive oxygen species that can alter cellular function. Moreover, DA depletion can attenuate dopaminergic cell loss in vitro. To test the contribution of DA to SN impairment in vivo, we used DA-deficient mice, which lack the enzyme tyrosine hydroxylase in dopaminergic cells, and mice pharmacologically depleted of DA by alpha -methyl-p-tyrosine pretreatment. Mice were treated with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), a toxin that produces parkinsonian pathology in humans, nonhuman primates, and rodents. In contrast to in vitro results, genetic or pharmacologic DA depletion did not attenuate loss of dopaminergic neurons in the SN or dopaminergic neuron terminals in the striatum. These results suggest that DA does not contribute to acute MPTP toxicity in vivo.
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Details
- Title
- Dopamine Depletion Does Not Protect against Acute 1-Methyl-4-Phenyl-1,2,3,6-Tetrahydropyridine Toxicity In Vivo
- Creators
- Daphne HasbaniFrancisco PerezRichard PalmiterKaren O'Malley
- Publication Details
- The Journal of neuroscience, v 25(41), pp 9428-9433
- Publisher
- Society for Neuroscience
- Resource Type
- Journal article
- Language
- English
- Academic Unit
- Pediatrics
- Web of Science ID
- WOS:000232546300013
- Scopus ID
- 2-s2.0-26844532113
- Other Identifier
- 991021838136604721
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- Collaboration types
- Domestic collaboration
- Web of Science research areas
- Neurosciences