The DOI matches its Crossref record; 10 of the 10 references it cites were found in a registry or an index.
α-Synuclein Overexpression in PC12 and Chromaffin Cells Impairs Catecholamine Release by Interfering with a Late Step in Exocytosis
Open accessAbstract
α-Synuclein (α-syn), a protein implicated in Parkinson's disease pathogenesis, is a presynaptic protein suggested to regulate transmitter release. We explored how α-syn overexpression in PC12 and chromaffin cells, which exhibit low endogenous α-syn levels relative to neurons, affects catecholamine release. Overexpression of wild-type or A30P mutant α-syn in PC12 cell lines inhibited evoked catecholamine release without altering calcium threshold or cooperativity of release. Electron micrographs revealed that vesicular pools were not reduced but that, on the contrary, a marked accumulation of morphologically “docked” vesicles was apparent in the α-syn-overexpressing lines. We used amperometric recordings from chromaffin cells derived from mice that overexpress A30P or wild-type (WT) α-syn, as well as chromaffin cells from control and α-syn null mice, to determine whether the filling of vesicles with the transmitter was altered. The quantal size and shape characteristics of amperometric events were identical for all mouse lines, suggesting that overexpression of WT or mutant α-syn did not affect vesicular transmitter accumulation or the kinetics of vesicle fusion. The frequency and number of exocytotic events per stimulus, however, was lower for both WT and A30P α-syn-overexpressing cells. The α-syn-overexpressing cells exhibited reduced depression of evoked release in response to repeated stimuli, consistent with a smaller population of readily releasable vesicles. We conclude that α-syn overexpression inhibits a vesicle “priming” step, after secretory vesicle trafficking to “docking” sites but before calcium-dependent vesicle membrane fusion.
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Cites
A neural substrate of prediction and reward
Schultz, W., Dayan, P., & Montague, P. R. (1997) · Science · doi:10.1126/science.275.5306.1593 · Cited by 9,388
Mutation in the α-Synuclein Gene Identified in Families with Parkinson's Disease
Polymeropoulos, M. H., Lavedan, C., Leroy, E., Ide, S. E., Dehejia, A., Dutra, A., Pike, B., Root, H., Rubenstein, J., Boyer, R., et al. (1997) · Science · doi:10.1126/science.276.5321.2045 · Cited by 8,240
AlaSOPro mutation in the gene encoding α-synuclein in Parkinson's disease
Krüger, R., Kuhn, W., Müller, T., Woitalla, D., Graeber, M., Kösel, S., Przuntek, H., Epplen, J. T., Schols, L., & Riess, O. (1998) · Nature Genetics · doi:10.1038/ng0298-106 · Cited by 3,836
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-citationIwai, A., Masliah, E., Yoshimoto, M., Ge, N., Flanagan, L., Rohan de Silva, H. A., Kittel, A., & Saitoh, T. (1995) · Neuron · doi:10.1016/0896-6273(95)90302-x · Cited by 1,316
A Role for α-Synuclein in the Regulation of Dopamine Biosynthesis
Perez, R. G., Waymire, J. C., Lin, E., Liu, J. J., Guo, F., & Zigmond, M. J. (2002) · The Journal of Neuroscience · doi:10.1523/jneurosci.22-08-03090.2002 · Cited by 598
The rat brain synucleins; family of proteins transiently associated with neuronal membrane
Maroteaux, L., & Scheller, R. H. (1991) · Molecular Brain Research · doi:10.1016/0169-328x(91)90043-w · Cited by 334
Peng, X. M., Tehranian, R., Dietrich, P., Stefanis, L., & Perez, R. G. (2005) · Journal of Cell Science · doi:10.1242/jcs.02481 · Cited by 249 · cited 3×
“…on effects of the protein on catecholamine synthesis, uptake, and vesicular accumulation (Lee et al., 2001; Lotharius et al., 2002; Perez et al., 2002; Wersinger et al., 2003; Peng et al., 2005), is that amount of transmitter released per vesicle fusion event (quantal size) might be decreased.”
BackgroundInfluentialSelf-citationα‐Synuclein produces a long‐lasting increase in neurotransmitter release
Liu, S., Ninan, I., Antonova, I., Battaglia, F., Trinchese, F., Narasanna, A., Kolodilov, N., Dauer, W., Hawkins, R. D., & Arancio, O. (2004) · The EMBO Journal · doi:10.1038/sj.emboj.7600451 · Cited by 198
α-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
-Synuclein in Parkinson's Disease
Stefanis, L. (2012) · Cold Spring Harbor Perspectives in Medicine · doi:10.1101/cshperspect.a009399 · Cited by 1,446
Self-citationBendor, J. T., Logan, T. P., & Edwards, R. H. (2013) · Neuron · doi:10.1016/j.neuron.2013.09.004 · Cited by 825
Self-citationMetals in Alzheimer's and Parkinson's Diseases
Barnham, K. J., & Bush, A. I. (2008) · Current Opinion in Chemical Biology · doi:10.1016/j.cbpa.2008.02.019 · Cited by 695
The Synaptic Function of α-Synuclein
Burré, J. (2015) · Journal of Parkinson's Disease · doi:10.3233/jpd-150642 · Cited by 573
Neuropathology, biochemistry, and biophysics of α‐synuclein aggregation
Uversky, V. N. (2007) · Journal of Neurochemistry · doi:10.1111/j.1471-4159.2007.04764.x · Cited by 567
Metadata
- Authors
- Larsen, K. E., Schmitz, Y., Troyer, M. D., Mosharov, E., Dietrich, P., Quazi, A. Z., Savalle, M., Nemani, V., Chaudhry, F. A., Edwards, R. H., Stefanis, L., & Sulzer, D.
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2006-11-15
- Volume
- 26
- Issue
- 46
- Pages
- 11915-11922
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- OpenAlex
- W1979944790
- Cited by
- 415
- References
- 10
- FWCI
- 12.34
- Type
- journal article
- Language
- en
- Open access
- hybrid
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- CoChat. (2026). Citation check: α-Synuclein Overexpression in PC12 and Chromaffin Cells Impairs Catecholamine Release by Interfering with a Late Step in Exocytosis. https://app.cochat.ai/papers/10.1523/jneurosci.3821-06.2006
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- Larsen, K. E., Schmitz, Y., Troyer, M. D., Mosharov, E., Dietrich, P., Quazi, A. Z., Savalle, M., Nemani, V., Chaudhry, F. A., Edwards, R. H., Stefanis, L., & Sulzer, D. (2006). α-Synuclein Overexpression in PC12 and Chromaffin Cells Impairs Catecholamine Release by Interfering with a Late Step in Exocytosis. The Journal of Neuroscience. https://doi.org/10.1523/jneurosci.3821-06.2006
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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.
