Abstract
We have investigated methamphetamine (MA) toxicity in transgenic mice that overexpress the human form of mitochondrial manganese superoxide dismutase (MnSOD). Our results reveal a significant reduction in the long-term depletion of striatal dopamine and protein oxidation following repeated administration of MA in transgenic vs. non-transgenic littermates. These findings support the notion that ROS contribute to MA-induced brain damage and suggest that mitochondria may play an important role in this form of neurodegeneration. (C) 2000 Elsevier Science B.V.
| Original language | English |
|---|---|
| Pages (from-to) | 218-222 |
| Number of pages | 5 |
| Journal | Brain Research |
| Volume | 878 |
| Issue number | 1-2 |
| DOIs | |
| State | Published - Sep 29 2000 |
Bibliographical note
Funding Information:This work was supported by USPHS Grants NS 01941 to WFM, CA 59835 to DKS, DA 10115 to WAC and AG 10836 to DAB. Electron micrographs were obtained using the University of Kentucky’s Image Facility with the assistance of Ms. Mary Gail Engle.
Funding
This work was supported by USPHS Grants NS 01941 to WFM, CA 59835 to DKS, DA 10115 to WAC and AG 10836 to DAB. Electron micrographs were obtained using the University of Kentucky’s Image Facility with the assistance of Ms. Mary Gail Engle.
| Funders | Funder number |
|---|---|
| National Institute on Drug Abuse | R29DA010115 |
| U.S. Public Health Service | CA 59835, AG 10836, NS 01941 |
Keywords
- Dopamine
- Manganese superoxide dismutase
- Methamphetamine
- Oxidative stress
- Striatum
- Transgenic mouse
ASJC Scopus subject areas
- General Neuroscience
- Molecular Biology
- Clinical Neurology
- Developmental Biology
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