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Eric C. Beattie,1David Stellwagen,1Wade Morishita,1Jacqueline C. Bresnahan,2Byeong Keun Ha,2Mark Von Zastrow,3Michael S. Beattie,2*Robert C. Malenka1*
Activity-dependent modulation of synaptic efficacy in the brain
contributes to neural circuit development and experience-dependentplasticity. Although glia are affected by activity and ensheathesynapses, their influence on synaptic strength has largely beenignored. Here, we show that a protein produced by glia, tumornecrosis
factor (TNF), enhances synaptic efficacy by increasingsurface expression of AMPA receptors. Preventing the actions ofendogenous TNF has the opposite effects. Thus, the continualpresence of TNF is required for preservation of synaptic strengthat
excitatory synapses. Through its effects on AMPA receptor trafficking,TNF may play roles in synaptic plasticity and modulating responsesto 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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NEUROSCIENCE: New Insights into Neuron-Glia Communication.