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Updated: May 29, 2026

Determination of Mitochondrial Membrane Potential and Reactive Oxygen Species in Live Rat Cortical Neurons
Published on: May 23, 2011
Reactive oxygen species and the neuronal fate
Karen A M Kennedy1, Shelley D E Sandiford, Ilona S Skerjanc
1Department of Biochemistry, Medical Sciences Building, The University of Western Ontario, London, ON, Canada.
Abstract:
Aberrant or elevated levels of reactive oxygen species (ROS) can mediate deleterious cellular effects, including neuronal toxicity and degeneration observed in the etiology of a number of pathological conditions, including Alzheimer's and Parkinson's diseases. Nevertheless, ROS can be generated in a controlled manner and can regulate redox sensitive transcription factors such as NFκB, AP-1 and NFAT. Moreover, ROS can modulate the redox state of tyrosine phosphorylated proteins, thereby having an impact on many transcriptional networks and signaling cascades important for neurogenesis. A large body of literature links the controlled generation of ROS at low-to-moderate levels with the stimulation of differentiation in certain developmental programs such as neurogenesis. In this regard, ROS are involved in governing the acquisition of the neural fate-from neural induction to the elaboration of axons. Here, we summarize and discuss the growing body of literature that describe a role for ROS signaling in neuronal development.
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