Get access

Role of reactive oxygen species in hippocampal long-term potentiation: Contributory or inhibitory?

Authors

  • Lauren T. Knapp,

    1. Department of Molecular Physiology and Biophysics and Division of Neuroscience, Baylor College of Medicine, Houston, Texas
    Search for more papers by this author
  • Eric Klann

    Corresponding author
    1. Department of Molecular Physiology and Biophysics and Division of Neuroscience, Baylor College of Medicine, Houston, Texas
    • Department of Molecular Physiology and Biophysics, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030
    Search for more papers by this author

Abstract

Reactive oxygen species (ROS) typically are characterized as molecules involved in neurotoxicity and neurodegeneration. However, recent evidence from both neuronal and nonneuronal cells suggests that ROS also function as small messenger molecules that are normal components of signal transduction cascades during physiological processes. Consistent with this idea, ROS have been shown to be critical for hippocampal long-term potentiation (LTP), a form of synaptic plasticity widely studied as a cellular substrate for learning and memory. On the other hand, ROS also have been shown to be involved in aging-related impairment of LTP. This review discusses the evidence supporting the notion that ROS both contribute to normal LTP and are involved in age-related impairment of LTP. We also discuss possible sources that might be responsible for the production of ROS after the induction of LTP. Finally, we propose a functional ROS continuum to help explain this dichotomy of ROS function in hippocampal LTP. © 2002 Wiley-Liss, Inc.

Ancillary