Journal
SCIENCE
Volume 295, Issue 5563, Pages 2282-2285Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1067859
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Funding
- NIDA NIH HHS [DA00439] Funding Source: Medline
- NIMH NIH HHS [MH063394] Funding Source: Medline
- NINDS NIH HHS [NS38079, NS 31193] Funding Source: Medline
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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.
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