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.
Copyright 2002 Wiley-Liss, Inc.