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Cited by 137Parkinson's Disease Mechanisms and TreatmentsNuclear Receptors and SignalingNerve injury and regeneration

Effects of 6-hydroxydopamine on primary cultures of substantia nigra: specific damage to dopamine neurons and the impact of glial cell line-derived neurotrophic factor

Ding, Yun Min, Jaumotte, Juliann D., Signore, Armando P., Zigmond, Michael J.·2004·Journal of Neurochemistry
DOI 10.1111/j.1471-4159.2004.02415.x
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Abstract

6-Hydroxydopamine (6-OHDA)-induced loss of dopamine (DA) neurons has served to produce an animal model of DA neuron loss in Parkinson's disease. We report here the use of 6-OHDA to produce an in vitro model of this phenomena using dissociated cultures prepared from neonatal rat mesencephalon. Cultures were exposed to 6-OHDA (40-100 microm, 15 min) in an antioxidant medium, and DA and GABA neurons evaluated by immunocytochemistry. 6-OHDA induced morphological and biochemical signs of cell death in DA neurons within 3 h, followed by loss of tyrosine hydroxylase immunoreactive neurons within 2 days. In substantia nigra (SN) cultures, DA neurons were much more affected by 6-OHDA than were GABA neurons. In contrast, DA neurons from the ventral tegmental area were only lost at higher, non-specific concentrations of 6-OHDA. The effects of 6-OHDA on nigral DA neurons were blocked by inhibitors of high affinity DA transport and by z-DEVD-fmk (150 microm), a caspase inhibitor. Glial cell line-derived neurotrophic factor (GDNF) treatment reduced TUNEL labeling 3 h after 6-OHDA exposure, but did not prevent loss of DA neurons at 48 h. Thus, 6-OHDA can selectively destroy DA neurons in post-natal cultures of SN, acting at least in part by initiating caspase-dependent apoptosis, and this effect can be attenuated early but not late by GDNF.

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Crossref · 10.1111/j.1471-4159.2004.02415.x

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  • In certain circumstances, neuroinflammation can help stimulate myelin repair or remove toxic aggregated proteins and cell debris from the CNS.

    “However, in certain circumstances, the neuroinflammation can help stimulate myelin repair or remove toxic aggregated proteins and cell debris from CNS (Ding et al., 2004; Simard et al., 2006; Glezer et al., 2007).”

    From The role of microglia in retinal neurodegeneration: Alzheimer’s disease, parkinson, and glaucoma. (2017) · cites this paper as Ding et al., 2004

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Authors
Ding, Y. M., Jaumotte, J. D., Signore, A. P., & Zigmond, M. J.
Affiliations
University of Pittsburgh (US)
ORCID
Venue
Journal of Neurochemistry
Publisher
Wiley
Published
2004-03-30
Volume
89
Issue
3
Pages
776-787
ISSN
  • 0022-3042 (ISSN-L)
  • 1471-4159
DOI
10.1111/j.1471-4159.2004.02415.x
OpenAlex
W2077764660
Cited by
137
References
78
Citations by year
2025: 1 · 2024: 3 · 2023: 3 · 2022: 11 · 2021: 1 · 2020: 11 · 2019: 7 · 2018: 8 · 2017: 7 · 2016: 5 · 2015: 6 · 2014: 6 · 2013: 10 · 2012: 5
FWCI
5.69
Type
journal article
Language
en
Open access
closed
Licence
onlinelibrary.wiley.com/termsAndConditions#vor (vor)
Locations
  • Journal of Neurochemistry (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health (5r01ns039267-05)
  • National Institute of Neurological Disorders and Stroke (NS 19608, NS39267)
Topics
  • Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nuclear Receptors and Signaling
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nerve injury and regeneration
Keywords
6-hydroxydopamine, substantia nigra, dopaminergic neurons, Parkinson's disease model, glial cell line-derived neurotrophic factor, caspase-dependent apoptosis, dopamine transporter, GABAergic neurons, ventral tegmental area, tyrosine hydroxylase, neuronal cell death, in vitro neuronal culture
MeSH terms
Animals, Cell Survival, Cells, Cultured, Enzyme Inhibitors, Membrane Glycoproteins, Models, Biological, Nerve Growth Factors, Nerve Tissue Proteins, Neurons, Substantia Nigra, Oxidopamine, Rats, Sprague-Dawley, Apoptosis, Ventral Tegmental Area, Neuroprotective Agents, Dopamine Uptake Inhibitors, Membrane Transport Proteins, Membrane Transport Modulators, Dopamine Plasma Membrane Transport Proteins, Glial Cell Line-Derived Neurotrophic Factor, Rats

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