Abrogating mitochondrial ROS in neurons or astrocytes reveals cell-specific impact on mouse behaviour

Cells naturally produce mitochondrial reactive oxygen species (mROS), but the in vivo pathophysiological significance has long remained controversial. Within the brain, astrocyte-derived mROS physiologically regulate behaviour and are produced at one order of magnitude faster than in neurons. Howeve...

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Bibliographic Details
Published in:Redox biology 2021-05, Vol.41, p.101917, Article 101917
Main Authors: Vicente-Gutierrez, Carlos, Bonora, Nicolo, Jimenez-Blasco, Daniel, Lopez-Fabuel, Irene, Bates, Georgina, Murphy, Michael P., Almeida, Angeles, Bolaños, Juan P.
Format: Article
Language:English
Subjects:
Animals
Astrocyte
Astrocytes - metabolism
Cells, Cultured
In vivo
Mice
Mitochondria
Neuron
Neurons
Reactive Oxygen Species - metabolism
ROS
Short Communication
Signallling
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Summary:Cells naturally produce mitochondrial reactive oxygen species (mROS), but the in vivo pathophysiological significance has long remained controversial. Within the brain, astrocyte-derived mROS physiologically regulate behaviour and are produced at one order of magnitude faster than in neurons. However, whether neuronal mROS abundance differentially impacts on behaviour is unknown. To address this, we engineered genetically modified mice to down modulate mROS levels in neurons in vivo. Whilst no alterations in motor coordination were observed by down modulating mROS in neurons under healthy conditions, it prevented the motor discoordination caused by the pro-oxidant neurotoxin, 3-nitropropionic acid (3-NP). In contrast, abrogation of mROS in astrocytes showed no beneficial effect against the 3-NP insult. These data indicate that the impact of modifying mROS production on mouse behaviour critically depends on the specific cell-type where they are generated.
ISSN:2213-2317
2213-2317
DOI:10.1016/j.redox.2021.101917