The generation of abnormally high levels of reactive oxygen species (ROS) is linked to cellular dysfunction, including neuronal toxicity and neurodegeneration. However, physiological ROS production modulates redox-sensitive roles of several molecules such as transcription factors, signaling proteins, and cytoskeletal components. Changes in the functions of redox-sensitive proteins may be important for defining key aspects of stem cell proliferation and differentiation, neuronal maturation, and neuronal plasticity. In neurons, most of the studies have been focused on the pathological implications of such modifications and only very recently their essential roles in neuronal development and plasticity has been recognized. In this review, we discuss the participation of NADPH oxidases (NOXs) and a family of protein-methionine sulfoxide oxidases, named molecule interacting with CasLs, as regulated enzymatic sources of ROS production in neurons, and describes the contribution of ROS signaling to neurogenesis and differentiation, neurite outgrowth, and neuronal plasticity. We review the role of reactive oxygen species (ROS) in neurogenesis, axon growth, and guidance and NMDA-receptor-mediated plasticity, LTP, and memory. ROS participation is presented in the context of NADPH oxidase and MICAL functions and their importance for brain functions.
Keywords: MICAL; NADPH oxidase; NMDA receptor; neural progenitor cells; neuronal differentiation; reactive oxygen species.
© 2016 International Society for Neurochemistry.