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

Fecha de publicación: 01/05/2021

Autores de IBSAL

• Carlos Vicente Gutiérrez

  Autor

• Daniel Jiménez Blasco

  Autor

• Irene López Fabuel

  Autor

• 

  Ángeles Almeida Parra

  Autor

• 

  Juan Pedro Bolaños Hernández

  Autor

Autores ajenos a IBSAL

• Bonora, N
• Bates, G
• Murphy, MP

Grupos

• IIMD-14 - Neuroenergética y Metabolismo

  

  Investigador Principal

  Juan Pedro Bolaños Hernández

• NEUR-03 - Neurobiología Molecular

  

  Investigador Principal

  Ángeles Almeida Parra

Abstract

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.

Keywords

• Mitochondria; ROS; Neuron; Astrocyte; Signallling; In vivo