The DOI matches its Crossref record; 69 of the 69 references it cites were found in a registry or an index.
Reduced Vesicular Storage of Dopamine Causes Progressive Nigrostriatal Neurodegeneration
Open accessAbstract
The vesicular monoamine transporter 2 (VMAT2; SLC18A2) is responsible for packaging dopamine into vesicles for subsequent release and has been suggested to serve a neuroprotective role in the dopamine system. Here, we show that mice that express ∼5% of normal VMAT2 (VMAT2 LO) display age-associated nigrostriatal dopamine dysfunction that ultimately results in neurodegeneration. Elevated cysteinyl adducts to l-DOPA and DOPAC are seen early and are followed by increased striatal protein carbonyl and 3-nitrotyrosine formation. These changes were associated with decreased striatal dopamine and decreased expression of the dopamine transporter and tyrosine hydroxylase. Furthermore, we observed an increase in α-synuclein immunoreactivity and accumulation and neurodegeneration in the substantia nigra pars compacta in aged VMAT2 LO mice. Thus, VMAT2 LO animals display nigrostriatal degeneration that begins in the terminal fields and progresses to eventual loss of the cell bodies, α-synuclein accumulation, and an l-DOPA responsive behavioral deficit, replicating many of the key aspects of Parkinson's disease. These data suggest that mishandling of dopamine via reduced VMAT2 expression is, in and of itself, sufficient to cause dopamine-mediated toxicity and neurodegeneration in the nigrostriatal dopamine system. In addition, the altered dopamine homeostasis resulting from reduced VMAT2 function may be conducive to pathogenic mechanisms induced by genetic or environmental factors thought to be involved in Parkinson's disease.
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Cites
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A Drosophila model of Parkinson's disease
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Oxidative stress in Parkinson's disease
Jenner, P. (2003) · Annals of Neurology · doi:10.1002/ana.10483 · Cited by 2,053
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Oxidative stress and Parkinson’s disease
Blesa, J., Trigo-Damas, I., Quiroga-Varela, A., & Jackson-Lewis, V. R. (2015) · Frontiers in Neuroanatomy · doi:10.3389/fnana.2015.00091 · Cited by 878
Mitochondrial dysfunction and mitophagy in parkinson’s disease: from mechanism to therapy
Malpartida, A. B., Williamson, M., Narendra, D. P., Wade-Martins, R., & Ryan, B. J. (2021) · Trends in Biochemical Sciences · doi:10.1016/j.tibs.2020.11.007 · Cited by 482
A Progressive Mouse Model of Parkinson’s Disease: The Thy1-aSyn (“Line 61”) Mice
Chesselet, M.-F., Richter, F., Zhu, C., Magen, I., Watson, M. B., & Subramaniam, S. R. (2012) · Neurotherapeutics · doi:10.1007/s13311-012-0104-2 · Cited by 346
Impaired dopamine metabolism in Parkinson’s disease pathogenesis
Masato, A., Plotegher, N., Boassa, D., & Bubacco, L. (2019) · Molecular Neurodegeneration · doi:10.1186/s13024-019-0332-6 · Cited by 328
Role of dopamine in the pathophysiology of Parkinson’s disease
Zhou, Z. D., Yi, L. X., Wang, D. Q., Lim, T. M., & Tan, E. K. (2023) · Translational Neurodegeneration · doi:10.1186/s40035-023-00378-6 · Cited by 308
Metadata
- Authors
- Caudle, W. M., Richardson, J. R., Wang, M. Z., Taylor, T. N., Guillot, T. S., McCormack, A. L., Colebrooke, R. E., Di Monte, D. A., Emson, P. C., & Miller, G. W.
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2007-07-25
- Volume
- 27
- Issue
- 30
- Pages
- 8138-8148
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- OpenAlex
- W2027822127
- Cited by
- 388
- References
- 69
- FWCI
- 13.51
- Type
- journal article
- Language
- en
- Open access
- hybrid
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- Caudle, W. M., Richardson, J. R., Wang, M. Z., Taylor, T. N., Guillot, T. S., McCormack, A. L., Colebrooke, R. E., Di Monte, D. A., Emson, P. C., & Miller, G. W. (2007). Reduced Vesicular Storage of Dopamine Causes Progressive Nigrostriatal Neurodegeneration. The Journal of Neuroscience. https://doi.org/10.1523/jneurosci.0319-07.2007
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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