Reactive Oxygen Species: Physiological and Physiopathological Effects on Synaptic Plasticity

DOI Web Site Web Site
  • Thiago Fernando Beckhauser
    Physiology and Biophysics Department, Biomedical Sciences Institute, Sao Paulo University (USP), Butanta, Sao Paulo, Brazil
  • José Francis-Oliveira
    Physiology and Biophysics Department, Biomedical Sciences Institute, Sao Paulo University (USP), Butanta, Sao Paulo, Brazil
  • Roberto De Pasquale
    Physiology and Biophysics Department, Biomedical Sciences Institute, Sao Paulo University (USP), Butanta, Sao Paulo, Brazil

書誌事項

タイトル別名
  • Supplementary Issue: Brain Plasticity and Repair

説明

<jats:p>In the mammalian central nervous system, reactive oxygen species (ROS) generation is counterbalanced by antioxidant defenses. When large amounts of ROS accumulate, antioxidant mechanisms become overwhelmed and oxidative cellular stress may occur. Therefore, ROS are typically characterized as toxic molecules, oxidizing membrane lipids, changing the conformation of proteins, damaging nucleic acids, and causing deficits in synaptic plasticity. High ROS concentrations are associated with a decline in cognitive functions, as observed in some neurodegenerative disorders and age-dependent decay of neuroplasticity. Nevertheless, controlled ROS production provides the optimal redox state for the activation of transductional pathways involved in synaptic changes. Since ROS may regulate neuronal activity and elicit negative effects at the same time, the distinction between beneficial and deleterious consequences is unclear. In this regard, this review assesses current research and describes the main sources of ROS in neurons, specifying their involvement in synaptic plasticity and distinguishing between physiological and pathological processes implicated.</jats:p>

収録刊行物

詳細情報 詳細情報について

問題の指摘

ページトップへ