The Journal of Neuroscience, September 1, 1999, 19(17):7241-7248
Reactive Oxygen Species Mediate Activity-Dependent Neuron-Glia
Signaling in Output Fibers of the Hippocampus
Coleen M.
Atkins and
J. David
Sweatt
Division of Neuroscience, Baylor College of Medicine, Houston,
Texas 77030
Nonsynaptic signaling is becoming increasingly appreciated in
studies of activity-dependent changes in the nervous system. We
investigated the types of neuronal activity that elicit nonsynaptic communication between neurons and glial cells in hippocampal output fibers. High-frequency, but not low-frequency, action potential firing
in myelinated CA1 axons of the hippocampus resulted in increased
phosphorylation of the oligodendrocyte-specific protein myelin basic
protein (MBP). This change was blocked by tetrodotoxin, indicating that
axonally generated action potentials were necessary to regulate the
phosphorylation state of MBP. Furthermore, scavengers of the reactive
oxygen species superoxide and hydrogen peroxide and nitric oxide
synthase inhibitors prevented activation of this neuron-glia signaling
pathway. These results indicate that, during periods of increased
neuronal activity in area CA1 of the hippocampus, reactive oxygen and
nitrogen species are generated, which diffuse to neighboring
oligodendrocytes and result in post-translational modifications of MBP,
a key structural protein in myelin. Thus, in addition to their
well-known capacity for activity-dependent neuron-neuron signaling,
hippocampal pyramidal neurons possess a mechanism for
activity-dependent neuron-glia signaling.
Key words:
hippocampus; oligodendrocyte; glia; myelin; myelin basic
protein; reactive oxygen species; superoxide; nitric oxide; hydrogen
peroxide; alveus; neuron-glia signaling
Copyright © 1999 Society for Neuroscience 0270-6474/99/19177241-08$05.00/0
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