Role for VGLUT2 in selective vulnerability of midbrain dopamine neurons
Open accessAbstract
Parkinson's disease is characterized by the loss of dopamine (DA) neurons in the substantia nigra pars compacta (SNc). DA neurons in the ventral tegmental area are more resistant to this degeneration than those in the SNc, though the mechanisms for selective resistance or vulnerability remain poorly understood. A key to elucidating these processes may lie within the subset of DA neurons that corelease glutamate and express the vesicular glutamate transporter VGLUT2. Here, we addressed the potential relationship between VGLUT expression and DA neuronal vulnerability by overexpressing VGLUT in DA neurons of flies and mice. In Drosophila, VGLUT overexpression led to loss of select DA neuron populations. Similarly, expression of VGLUT2 specifically in murine SNc DA neurons led to neuronal loss and Parkinsonian behaviors. Other neuronal cell types showed no such sensitivity, suggesting that DA neurons are distinctively vulnerable to VGLUT2 expression. Additionally, most DA neurons expressed VGLUT2 during development, and coexpression of VGLUT2 with DA markers increased following injury in the adult. Finally, conditional deletion of VGLUT2 made DA neurons more susceptible to Parkinsonian neurotoxins. These data suggest that the balance of VGLUT2 expression is a crucial determinant of DA neuron survival. Ultimately, manipulation of this VGLUT2-dependent process may represent an avenue for therapeutic development.
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Vglut2+ dopamine neurons in the substantia nigra pars compacta are particularly resistant to degeneration in toxin models of Parkinson's disease, and VGLUT2 may play a neuroprotective role by inducing a BDNF/TRKB dependent signaling cascade.
“In toxin models of PD, Vglut2+ DA neurons in the SNc are particularly resistant to degeneration [58,59], and VGLUT2 itself may play a neuroprotective role by inducing a BDNF/TRKB dependent signaling cascade [59].”
From Classification of midbrain dopamine neurons using single-cell gene expression profiling approaches (2020) · cites this paper as [58]
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- Authors
- Steinkellner, T., Zell, V., Farino, Z. J., Sonders, M. S., Villeneuve, M., Freyberg, R. J., Przedborski, S., Lu, W., Freyberg, Z., & Hnasko, T. S.
- Affiliations
- University of California San Diego (US)
- University of Pittsburgh (US)
- Columbia University (US)
- ORCID
- Venue
- Journal of Clinical Investigation
- Published
- 2018-01-16
- Volume
- 128
- Issue
- 2
- Pages
- 774-788
- ISSN
- 0021-9738 (ISSN-L)
- 1558-8238
- PMC
- PMC5785252
- OpenAlex
- W2783295659
- Cited by
- 102
- References
- 68
- Citations by year
- 2026: 9 · 2025: 14 · 2024: 15 · 2023: 14 · 2022: 6 · 2021: 15 · 2020: 10 · 2019: 12 · 2018: 7
- FWCI
- 7.46
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Locations
- Journal of Clinical Investigation (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- eScholarship (California Digital Library) (submittedVersion, cc-by-nc-nd)
- Funders
- NIH-NINDS (NIH-NINDS R21NS087496)
- Austrian Science Fund (J3656-B24)
- DOD PRMRP (PR141292)
- Topics
- Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nuclear Receptors and Signaling
- Keywords
- VGLUT2, vesicular glutamate transporter, dopaminergic neurons, Parkinson's disease, substantia nigra pars compacta, ventral tegmental area, selective neuronal vulnerability, Drosophila, conditional knockout, neuronal survival, neurodegeneration
- MeSH terms
- Animals, Disease Models, Animal, Dopamine, Drosophila melanogaster, Female, Humans, Male, Mesencephalon, Neurons, Neurotoxins, Parkinson Disease, Substantia Nigra, Ventral Tegmental Area, Glutamic Acid, Transgenes, Neurodegenerative Diseases, Vesicular Glutamate Transport Protein 2, Mice, Dopaminergic Neurons
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