The DOI matches its Crossref record; 9 of the 9 references it cites were found in a registry or an index.
Interplay between Cytosolic Dopamine, Calcium, and α-Synuclein Causes Selective Death of Substantia Nigra Neurons
Open accessAbstract
Summary The basis for selective death of specific neuronal populations in neurodegenerative diseases remains unclear. Parkinson's disease (PD) is a synucleinopathy characterized by a preferential loss of dopaminergic neurons in the substantia nigra (SN), whereas neurons of the ventral tegmental area (VTA) are spared. Using intracellular patch electrochemistry to directly measure cytosolic dopamine (DAcyt) in cultured midbrain neurons, we confirm that elevated DAcyt and its metabolites are neurotoxic and that genetic and pharmacological interventions that decrease DAcyt provide neuroprotection. L-DOPA increased DAcyt in SN neurons to levels 2-3-fold higher than in VTA neurons, a response dependent on dihydropyridine-sensitive Ca2+ channels, resulting in greater susceptibility of SN neurons to L-DOPA-induced neurotoxicity. DAcyt was not altered by α-synuclein deletion, although dopaminergic neurons lacking α-synuclein were resistant to L-DOPA-induced cell death. Thus, an interaction between Ca2+, DAcyt and α-synuclein may underlie the susceptibility of SN neurons in PD, suggesting multiple therapeutic targets.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Mice Lacking α-Synuclein Display Functional Deficits in the Nigrostriatal Dopamine System
Abeliovich, A., Schmitz, Y., Fariñas, I., Choi-Lundberg, D., Ho, W.-H., Castillo, P. E., Shinsky, N., Verdugo, J. M. G., Armanini, M., Ryan, A., et al. (2000) · Neuron · doi:10.1016/s0896-6273(00)80886-7 · Cited by 1,722
Self-citationMelanized dopaminergic neurons are differentially susceptible to degeneration in Parkinson's disease
Hirsch, E., Graybiel, A. M., & Agid, Y. A. (1988) · Nature · doi:10.1038/334345a0 · Cited by 1,301 · cited 1×
“Conversely, dopaminergic neurons in the VTA, which are spared in PD, produce minimal neuromelanin over a lifetime (Hirsch et al., 1988; Liang et al., 2004; Zecca et al., 2001).”
Catecholamine Metabolism: A Contemporary View with Implications for Physiology and Medicine
Eisenhofer, G., Kopin, I. J., & Goldstein, D. S. (2004) · Pharmacological Reviews · doi:10.1124/pr.56.3.1 · Cited by 1,072
Wightman, R. M., Jankowski, J. A., Kennedy, R. T., Kawagoe, K. T., Schroeder, T. J., Leszczyszyn, D. J., Near, J. A., Diliberto, E. J., & Viveros, O. H. (1991) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.88.23.10754 · Cited by 893
Expanding insights of mitochondrial dysfunction in Parkinson's disease
Abou-Sleiman, P. M., Muqit, M. M. K., & Wood, N. W. (2006) · Nature Reviews Neuroscience · doi:10.1038/nrn1868 · Cited by 869
Day, M., Wang, Z., Ding, J., An, X., Ingham, C. A., Shering, A. F., Wokosin, D., Ilijic, E., Sun, Z., Sampson, A. R., et al. (2006) · Nature Neuroscience · doi:10.1038/nn1632 · Cited by 745 · cited 2×
“, 2008), and a likely protective action of L-DOPA therapy on the striatopallidal pathway (Day et al., 2006).”
Tyrosine hydroxylase phosphorylation: Regulation and consequences
Dunkley, P. R., Bobrovskaya, L., Graham, M. E., Von Nagy‐Felsobuki, E. I., & Dickson, P. W. (2004) · Journal of Neurochemistry · doi:10.1111/j.1471-4159.2004.02797.x · Cited by 455 · cited 2×
“It should also be noted that Ca 2+ dependent phosphorylation of TH (Dunkley et al., 2004) is likely to play a role in the absence of exogenously added L-DOPA.”
Intraneuronal dopamine-quinone synthesis: a review
Sulzer, D., & Zecca, L. (1999) · Neurotoxicity Research · doi:10.1007/bf03033289 · Cited by 284
Self-citationα-Synuclein Overexpression Increases Cytosolic Catecholamine Concentration
Mosharov, E. V., Staal, R. G. W., Bové, J., Prou, D., Hananiya, A., Markov, D., Poulsen, N., Larsen, K. E., Moore, C. M. H., Troyer, M. D., et al. (2006) · The Journal of Neuroscience · doi:10.1523/jneurosci.0519-06.2006 · Cited by 165
Cited by
Poewe, W., Seppi, K., Tanner, C. M., Halliday, G. M., Brundin, P., Volkmann, J., Schrag, A.-E., & Lang, A. E. (2017) · Nature Reviews Disease Primers · doi:10.1038/nrdp.2017.13 · Cited by 5,415
The Role of Oxidative Stress in Parkinson's Disease
Dias, V., Junn, E., & Mouradian, M. M. (2013) · Journal of Parkinson’s Disease · doi:10.3233/jpd-130230 · Cited by 1,845
-Synuclein in Parkinson's Disease
Stefanis, L. (2012) · Cold Spring Harbor Perspectives in Medicine · doi:10.1101/cshperspect.a009399 · Cited by 1,446
Selective neuronal vulnerability in Parkinson disease
Surmeier, D. J., Obeso, J. A., & Halliday, G. M. (2017) · Nature Reviews Neuroscience · doi:10.1038/nrn.2016.178 · Cited by 1,116
Neuropathological assessment of Parkinson’s disease: refining the diagnostic criteria
Dickson, D. W., Braak, H., Duda, J. E., Duyckaerts, C., Gasser, T., Halliday, G. M., Hardy, J., Leverenz, J. B., Del Tredici, K., Wszolek, Z. K., et al. (2009) · The Lancet Neurology · doi:10.1016/s1474-4422(09)70238-8 · Cited by 972
Metadata
- Authors
- Mosharov, E. V., Larsen, K. E., Kanter, E., Phillips, K. A., Wilson, K., Schmitz, Y., Krantz, D. E., Kobayashi, K., Edwards, R. H., & Sulzer, D.
- Venue
- Neuron
- Publisher
- Elsevier BV
- Published
- 2009-04
- Volume
- 62
- Issue
- 2
- Pages
- 218-229
- ISSN
- 0896-6273 (ISSN-L)
- OpenAlex
- W2013503732
- Cited by
- 534
- References
- 9
- FWCI
- 23.06
- Type
- journal article
- Language
- en
- Open access
- bronze
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
How to cite
Cite CoChat for the checks on this page, and the paper for its own findings.
- This page
- CoChat. (2026). Citation check: Interplay between Cytosolic Dopamine, Calcium, and α-Synuclein Causes Selective Death of Substantia Nigra Neurons. https://app.cochat.ai/papers/10.1016/j.neuron.2009.01.033
- The paper
- Mosharov, E. V., Larsen, K. E., Kanter, E., Phillips, K. A., Wilson, K., Schmitz, Y., Krantz, D. E., Kobayashi, K., Edwards, R. H., & Sulzer, D. (2009). Interplay between Cytosolic Dopamine, Calcium, and α-Synuclein Causes Selective Death of Substantia Nigra Neurons. Neuron. https://doi.org/10.1016/j.neuron.2009.01.033
Data sources
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).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
