The DOI matches its Crossref record; 7 of the 7 references it cites were found in a registry or an index.
Increased striatal dopamine release and hyperdopaminergic‐like behaviour in mice lacking both alpha‐synuclein and gamma‐synuclein
Open accessAbstract
Alpha‐synuclein is intimately involved in the pathogenesis of Parkinson's disease, and has been implicated in the regulation of synthesis, release and reuptake of dopamine (DA). However, mice lacking members of the synuclein family have been reported to display no overt behavioural phenotype. This may be a result of compensatory upregulation of other synucleins during development. Here we report on behaviour and DA synapse function of alpha‐synuclein null, gamma‐synuclein null, and alpha‐gamma‐synuclein double‐null knockout mice. Double‐null mice were hyperactive in a novel environment and alternated at a lower rate in a T‐maze spontaneous alternation task, a phenotype reminiscent of mice expressing reduced levels of the DA transporter. To investigate a possible hyperdopaminergic phenotype in alpha‐gamma‐synuclein double‐null mice, we used fast‐scan cyclic voltammetry at carbon‐fibre microelectrodes to assess DA release and reuptake in striatal slices from wild‐type, alpha‐null, gamma‐null and double‐null mice in real time. Double‐null mice were found to have a twofold increase in the extracellular concentration of DA detected after discrete electrical stimuli in the striatum. By measuring the rate of reuptake of DA and tissue DA content in these animals, we showed that the observed increase in size of striatal DA transients was not attributable to a decrease in reuptake of DA via the DA transporter, and can not be attributed to an increase in tissue DA levels in the striatum. Rather, we propose that loss of both alpha‐ and gamma‐synuclein causes an increase in release probability from dopaminergic synapses.
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Cites
α-synuclein locus duplication as a cause of familial Parkinson's disease
Chartier-Harlin, M.-C., Kachergus, J., Roumier, C., Mouroux, V., Douay, X., Lincoln, S., Levecque, C., Larvor, L., Andrieux, J., Hulihan, M., et al. (2004) · The Lancet · doi:10.1016/s0140-6736(04)17103-1 · Cited by 2,029
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
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
Nicotine amplifies reward-related dopamine signals in striatum
Rice, M. E., & Cragg, S. J. (2004) · Nature Neuroscience · doi:10.1038/nn1244 · Cited by 594
Self-citationDouble-knockout mice for α- and β-synucleins: Effect on synaptic functions
Chandra, S., Fornai, F., Kwon, H.-B., Yazdani, U., Atasoy, D., Liu, X., Hammer, R. E., Battaglia, G., German, D. C., Castillo, P. E., et al. (2004) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0406283101 · Cited by 438
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 2×
“In tissue culture models, alpha-synuclein has been shown to inhibit DA synthesis by regulating the activity of tyrosine hydroxylase, protein phosphotase 2A, and aromatic amino acid decarboxylase (Perez et al., 2002; Peng et al., 2005; Tehranian et al., 2006).”
BackgroundNinkina, N., Papachroni, K., Robertson, D. C., Schmidt, O., Delaney, L., O'Neill, F., Court, F., Rosenthal, A., Fleetwood-Walker, S. M., Davies, A. M., et al. (2003) · Molecular and Cellular Biology · doi:10.1128/mcb.23.22.8233-8245.2003 · Cited by 75
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Cited by
Bendor, J. T., Logan, T. P., & Edwards, R. H. (2013) · Neuron · doi:10.1016/j.neuron.2013.09.004 · Cited by 825
Cell Biology and Pathophysiology of α-Synuclein
Burré, J., Sharma, M., & Südhof, T. C. (2018) · Cold Spring Harbor Perspectives in Medicine · doi:10.1101/cshperspect.a024091 · Cited by 579
The Synaptic Function of α-Synuclein
Burré, J. (2015) · Journal of Parkinson's Disease · doi:10.3233/jpd-150642 · Cited by 573
Striatal dopamine neurotransmission: Regulation of release and uptake
Sulzer, D., Cragg, S. J., & Rice, M. E. (2016) · Basal Ganglia · doi:10.1016/j.baga.2016.02.001 · Cited by 382
Self-citationDeficits in dopaminergic transmission precede neuron loss and dysfunction in a new Parkinson model
Janezic, S., Threlfell, S., Dodson, P. D., Dowie, M. J., Taylor, T. N., Potgieter, D., Parkkinen, L., Senior, S. L., Anwar, S., Ryan, B., et al. (2013) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1309143110 · Cited by 344
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Metadata
- Authors
- Senior, S. L., Ninkina, N., Deacon, R., Bannerman, D., Buchman, V. L., Cragg, S. J., & Wade‐Martins, R.
- Venue
- European Journal of Neuroscience
- Publisher
- Wiley
- Published
- 2008-02
- Volume
- 27
- Issue
- 4
- Pages
- 947-957
- ISSN
- 0953-816X (ISSN-L)
- 1460-9568
- OpenAlex
- W2080566347
- Cited by
- 164
- References
- 7
- FWCI
- 6.09
- Type
- journal article
- Language
- en
- Open access
- green
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- Senior, S. L., Ninkina, N., Deacon, R., Bannerman, D., Buchman, V. L., Cragg, S. J., & Wade‐Martins, R. (2008). Increased striatal dopamine release and hyperdopaminergic‐like behaviour in mice lacking both alpha‐synuclein and gamma‐synuclein. European Journal of Neuroscience. https://doi.org/10.1111/j.1460-9568.2008.06055.x
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