Abstract
The nematode Caenorhabditis elegans is a powerful genetic model that can be used to investigate neuronal death. Research using C. elegans has been crucial to characterize cell death programmes that are conserved in mammals. Many neuronal signaling components, such as those mediating dopaminergic neurotransmission, are preserved as well. Dopaminergic neurons are progressively lost in Parkinson's disease and an important risk factor to develop this disease appears to be oxidative stress, the increased occurrence of highly reactive oxygen species. Oxidative stress-induced dopaminergic neurodegeneration is mimicked in animal models by treatment with 6-hydroxydopamine (6-OHDA), a dopamine analog, which is specifically taken up into dopaminergic neurons. After exposing C. elegans to 6-OHDA, the loss of fluorescently labeled dopaminergic neurons can be easily monitored. An organisms' sensitivity to oxidative stress is thought to be influenced by basal levels of intrinsic oxidative stress and the ability to counteract oxidative stress and oxidative stress-induced damage. The C. elegans '6-OHDA model' led to the discovery of novel genes that are required to protect dopaminergic neurons and it has helped to determine the effects of conserved cell death and cell engulfment pathways in dopaminergic neurodegeneration. Here, we describe a simple protocol that allows for the easy detection of dopaminergic neuron loss after 6-OHDA treatment in C. elegans.
| Language | English |
|---|---|
| Article number | e3025 |
| Number of pages | 12 |
| Journal | Bio-Protocol |
| Volume | 8 |
| Issue number | 18 |
| DOIs | |
| Publication status | Published - 20 Sep 2018 |
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Keywords
- C. elegans
- Caenorhabditis elegans
- 6-OHDA
- 6-hydroxydopamine
- Oxidative stress assay
- Intoxication
- Dopaminergic neurodegeneration
Cite this
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6-hydroxydopamine (6-OHDA) Oxidative Stress Assay for Observing Dopaminergic Neuron Loss in Caenorhabditis elegans. / Offenburger, Sarah-Lena (Lead / Corresponding author); Gartner, Anton.
In: Bio-Protocol, Vol. 8, No. 18, e3025, 20.09.2018.Research output: Contribution to journal › Article
TY - JOUR
T1 - 6-hydroxydopamine (6-OHDA) Oxidative Stress Assay for Observing Dopaminergic Neuron Loss in Caenorhabditis elegans
AU - Offenburger, Sarah-Lena
AU - Gartner, Anton
N1 - Wellcome trust grant to AG (0909444/Z/09/Z and a Parkinson's UK Grant (G0912) together with a Wellcome Trust Strategic award (097045/B/11/Z). We acknowledge the Dundee Imaging Facility which is supported by the Wellcome Trust Technology Platform award (097945/B/11/Z) and the MRC Next Generation Optical Microscopy award (MR/K015869/1). SLO was supported by a PhD from the Molecular and Cellular Biology programme funded by the Wellcome Trust and by ISSF funding from the Wellcome Trust. Some strains were provided by the CGC, which is funded by the NIH Office of Research Infrastructure Programs (P40 OD010440).
PY - 2018/9/20
Y1 - 2018/9/20
N2 - The nematode Caenorhabditis elegans is a powerful genetic model that can be used to investigate neuronal death. Research using C. elegans has been crucial to characterize cell death programmes that are conserved in mammals. Many neuronal signaling components, such as those mediating dopaminergic neurotransmission, are preserved as well. Dopaminergic neurons are progressively lost in Parkinson's disease and an important risk factor to develop this disease appears to be oxidative stress, the increased occurrence of highly reactive oxygen species. Oxidative stress-induced dopaminergic neurodegeneration is mimicked in animal models by treatment with 6-hydroxydopamine (6-OHDA), a dopamine analog, which is specifically taken up into dopaminergic neurons. After exposing C. elegans to 6-OHDA, the loss of fluorescently labeled dopaminergic neurons can be easily monitored. An organisms' sensitivity to oxidative stress is thought to be influenced by basal levels of intrinsic oxidative stress and the ability to counteract oxidative stress and oxidative stress-induced damage. The C. elegans '6-OHDA model' led to the discovery of novel genes that are required to protect dopaminergic neurons and it has helped to determine the effects of conserved cell death and cell engulfment pathways in dopaminergic neurodegeneration. Here, we describe a simple protocol that allows for the easy detection of dopaminergic neuron loss after 6-OHDA treatment in C. elegans.
AB - The nematode Caenorhabditis elegans is a powerful genetic model that can be used to investigate neuronal death. Research using C. elegans has been crucial to characterize cell death programmes that are conserved in mammals. Many neuronal signaling components, such as those mediating dopaminergic neurotransmission, are preserved as well. Dopaminergic neurons are progressively lost in Parkinson's disease and an important risk factor to develop this disease appears to be oxidative stress, the increased occurrence of highly reactive oxygen species. Oxidative stress-induced dopaminergic neurodegeneration is mimicked in animal models by treatment with 6-hydroxydopamine (6-OHDA), a dopamine analog, which is specifically taken up into dopaminergic neurons. After exposing C. elegans to 6-OHDA, the loss of fluorescently labeled dopaminergic neurons can be easily monitored. An organisms' sensitivity to oxidative stress is thought to be influenced by basal levels of intrinsic oxidative stress and the ability to counteract oxidative stress and oxidative stress-induced damage. The C. elegans '6-OHDA model' led to the discovery of novel genes that are required to protect dopaminergic neurons and it has helped to determine the effects of conserved cell death and cell engulfment pathways in dopaminergic neurodegeneration. Here, we describe a simple protocol that allows for the easy detection of dopaminergic neuron loss after 6-OHDA treatment in C. elegans.
KW - C. elegans
KW - Caenorhabditis elegans
KW - 6-OHDA
KW - 6-hydroxydopamine
KW - Oxidative stress assay
KW - Intoxication
KW - Dopaminergic neurodegeneration
U2 - 10.21769/BioProtoc.3025
DO - 10.21769/BioProtoc.3025
M3 - Article
VL - 8
JO - Bio-Protocol
T2 - Bio-Protocol
JF - Bio-Protocol
SN - 2331-8325
IS - 18
M1 - e3025
ER -