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Synaptic Microcircuit Modeling with 3D Cocultures of Astrocytes and Neurons from Human Pluripotent Stem Cells
Published on: August 16, 2018
More than a sidekick: glia and homeostatic synaptic plasticity
1Department of Biology, Brandeis University, Waltham, MA 02454, USA. turrigiano@brandeis.edu
Trends in Molecular Medicine
|August 26, 2006
Summary
Glial cells release tumor necrosis factor-alpha (TNF-alpha), a cytokine that drives synaptic scaling. This finding reveals a novel mechanism for homeostatic plasticity, highlighting a partnership between glia and neurons.
Area of Science:
- Neuroscience
- Cellular Biology
- Synaptic Plasticity
Background:
- Homeostatic synaptic plasticity stabilizes neural network activity.
- The precise mechanisms underlying homeostatic plasticity remain largely unknown.
- Tumor necrosis factor-alpha (TNF-alpha) is implicated in synaptic function.
Purpose of the Study:
- To investigate the mechanisms of homeostatic synaptic plasticity.
- To identify the source of TNF-alpha involved in synaptic scaling.
- To elucidate the roles of glia and neurons in synaptic plasticity.
Main Methods:
- Activity-dependent induction of synaptic scaling.
- Measurement of TNF-alpha release.
- Distinguishing between glial and neuronal sources of TNF-alpha.
Main Results:
- Synaptic scaling is induced by activity-dependent release of TNF-alpha.
- The primary source of TNF-alpha in this process is glial cells, not neurons.
- These findings provide new insights into the regulation of synaptic strength.
Conclusions:
- Glial cells play a critical role in homeostatic synaptic plasticity through TNF-alpha release.
- This study establishes an equal partnership between glial cells and neurons in generating synaptic plasticity.
- The findings advance our understanding of neural network stability and function.
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