Synaptic Vesicle Depletion Correlates with Attenuated Synaptic Responses to Prolonged Repetitive Stimulation in Mice Lacking α-Synuclein
Open accessAbstract
Although the mutation of alpha-synuclein, a protein associated with presynaptic vesicles, is implicated in the etiology and pathogenesis of Parkinson's disease, the biological function of the normal protein is unknown. Mice that lack alpha-synuclein have been generated by homologous recombination in embryonic stem cells. Electron microscopic examination of hippocampal synapses revealed a striking selective deficiency of undocked vesicles without affecting docked vesicles. Field recording of CA1 synapses in hippocampal slices from the mutant mice demonstrated normal basal synaptic transmission, paired-pulse facilitation, and response to a brief train of high-frequency stimulation (100 Hz, 40 pulses) that exhausts only docked vesicles. In contrast, the alpha-synuclein knock-out mice exhibited significant impairments in synaptic response to a prolonged train of repetitive stimulation (12.5 Hz, 300 pulses) capable of depleting docked as well as reserve pool vesicles. Moreover, the replenishment of the docked vesicles by reserve pool vesicles after depletion was slower in the mutant synapses. Thus, alpha-synuclein may be required for the genesis and/or maintenance of a subset of presynaptic vesicles, those in the "reserve" or "resting" pools. These results reveal, for the first time, the normal function of endogenous alpha-synuclein in regulating synaptic vesicle mobilization at nerve terminals.
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αSyn-KO and α/β-Syn double-KO mice exhibit reduced brain dopamine levels compared to wild-type animals.
“However, αSyn-KO, and α/β-Syn double-KO mice exhibited reduced brain dopamine levels compared to wild-type (wt) animals”
From α-synuclein in the pathophysiology of Alzheimer’s disease (2019) · cites this paper as [156]
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- Authors
- Cabin, D. E., Shimazu, K., Murphy, D., Cole, N. B., Gottschalk, W., McIlwain, K. L., Orrison, B., Chen, A., Ellis, C. E., Paylor, R., Lu, B., & Nussbaum, R. L.
- Affiliations
- National Institutes of Health (US)
- National Human Genome Research Institute (US)
- Baylor College of Medicine (US)
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2002-10-15
- Volume
- 22
- Issue
- 20
- Pages
- 8797-8807
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC6757677
- OpenAlex
- W1502551601
- Cited by
- 865
- References
- 47
- Citations by year
- 2026: 23 · 2025: 30 · 2024: 20 · 2023: 23 · 2022: 43 · 2021: 35 · 2020: 34 · 2019: 35 · 2018: 31 · 2017: 34 · 2016: 32 · 2015: 40 · 2014: 39 · 2013: 42 · 2012: 38
- FWCI
- 22.57
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Neuroscience (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Human Genome Research Institute
- National Institute of Child Health and Human Development
- Topics
- Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Cellular transport and secretion
- Keywords
- alpha-synuclein, synaptic vesicle depletion, reserve pool, docked vesicles, presynaptic vesicles, paired-pulse facilitation, high-frequency stimulation, hippocampal CA1 synapses, Parkinson's disease, synaptic transmission
- MeSH terms
- Amphetamine, Animals, Behavior, Animal, Calcium, Cells, Cultured, Crosses, Genetic, Electric Stimulation, Heterozygote, Hippocampus, Male, Motor Activity, Nerve Tissue Proteins, Synaptic Transmission, Neurons, Synapses, Synaptic Vesicles, Synaptosomes, Immunoblotting, Blotting, Western, Presynaptic Terminals, Mice, Knockout, Excitatory Postsynaptic Potentials, Mice, Synucleins, alpha-Synuclein
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