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Science 295 (5563): 2282-2285

Copyright © 2002 by the American Association for the Advancement of Science

Control of Synaptic Strength by Glial TNFalpha

Eric C. Beattie,1 David Stellwagen,1 Wade Morishita,1 Jacqueline C. Bresnahan,2 Byeong Keun Ha,2 Mark Von Zastrow,3 Michael S. Beattie,2* Robert C. Malenka1*

Activity-dependent modulation of synaptic efficacy in the brain contributes to neural circuit development and experience-dependent plasticity. Although glia are affected by activity and ensheathe synapses, their influence on synaptic strength has largely been ignored. Here, we show that a protein produced by glia, tumor necrosis factor alpha  (TNFalpha ), enhances synaptic efficacy by increasing surface expression of AMPA receptors. Preventing the actions of endogenous TNFalpha has the opposite effects. Thus, the continual presence of TNFalpha is required for preservation of synaptic strength at excitatory synapses. Through its effects on AMPA receptor trafficking, TNFalpha may play roles in synaptic plasticity and modulating responses to neural injury.

1 Nancy Pritzker Laboratory, Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Palo Alto, CA 94304, USA.
2 Department of Neuroscience, The Ohio State University Medical Center, Columbus, OH 43210, USA.
3 Departments of Psychiatry and Cellular and Molecular Pharmacology, University of California, San Francisco, CA 94143, USA.
*   To whom correspondence should be addressed. E-mail: beattie.2{at}osu.edu (M.S.B.); malenka{at}stanford.edu (R.C.M.)

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