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Synaptic scaling mediated by glial TNF-α

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  • David Stellwagen

    (Stanford University School of Medicine)

  • Robert C. Malenka

    (Stanford University School of Medicine)

Abstract

Two general forms of synaptic plasticity that operate on different timescales are thought to contribute to the activity-dependent refinement of neural circuitry during development: (1) long-term potentiation (LTP) and long-term depression (LTD), which involve rapid adjustments in the strengths of individual synapses in response to specific patterns of correlated synaptic activity, and (2) homeostatic synaptic scaling, which entails uniform adjustments in the strength of all synapses on a cell in response to prolonged changes in the cell's electrical activity1,2. Without homeostatic synaptic scaling, neural networks can become unstable and perform suboptimally1,2,3. Although much is known about the mechanisms underlying LTP and LTD4, little is known about the mechanisms responsible for synaptic scaling except that such scaling is due, at least in part, to alterations in receptor content at synapses5,6,7. Here we show that synaptic scaling in response to prolonged blockade of activity is mediated by the pro-inflammatory cytokine tumour-necrosis factor-α (TNF-α). Using mixtures of wild-type and TNF-α-deficient neurons and glia, we also show that glia are the source of the TNF-α that is required for this form of synaptic scaling. We suggest that by modulating TNF-α levels, glia actively participate in the homeostatic activity-dependent regulation of synaptic connectivity.

Suggested Citation

  • David Stellwagen & Robert C. Malenka, 2006. "Synaptic scaling mediated by glial TNF-α," Nature, Nature, vol. 440(7087), pages 1054-1059, April.
  • Handle: RePEc:nat:nature:v:440:y:2006:i:7087:d:10.1038_nature04671
    DOI: 10.1038/nature04671
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    Cited by:

    1. Shun Li & Florian olde Heuvel & Rida Rehman & Oumayma Aousji & Albrecht Froehlich & Zhenghui Li & Rebecca Jark & Wanhong Zhang & Alison Conquest & Sarah Woelfle & Michael Schoen & Caitlin C. O´Meara &, 2023. "Interleukin-13 and its receptor are synaptic proteins involved in plasticity and neuroprotection," Nature Communications, Nature, vol. 14(1), pages 1-21, December.
    2. Hang Zhou & Guo-Qiang Bi & Guosong Liu, 2024. "Intracellular magnesium optimizes transmission efficiency and plasticity of hippocampal synapses by reconfiguring their connectivity," Nature Communications, Nature, vol. 15(1), pages 1-20, December.

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