Abstract
Since it was first described almost 30 years ago, homeostatic synaptic plasticity (HSP) has been hypothesized to play a key role in maintaining neuronal circuit function in both developing and adult animals. While well characterized in vitro, determining the in vivo roles of this form of plasticity remains challenging. Since the discovery that the pro-inflammatory cytokine tumor necrosis factor-α (TNF-α) mediates some forms of HSP, it has been possible to probe some of the in vivo contribution of TNF-mediated HSP. Work from our lab and others has found roles for TNF-HSP in a variety of functions, including the developmental plasticity of sensory systems, models of drug addiction, and the response to psychiatric drugs.
Highlights
We suggest that tumor necrosis factor (TNF) may play a similar pleiotropic role in regulating neuronal circuit function
It is clear that the effects of TNF on neurotransmission are neuronal subtype-specific, and that it can lead to several different outcomes at the level of synapses
The common thread is that these changes still appear to normalize circuit output in response to perturbing stimuli, which is consistent with TNF being a mediator of homeostatic synaptic plasticity (HSP)
Summary
Department of Neurology and Neurosurgery, Centre for Research in Neuroscience, Research Institute of the McGill University Health Center, Montréal, QC, Canada Reviewed by: Thomas Deller, Goethe University Frankfurt, Germany Igor Delvendahl, University of Zurich, Switzerland Specialty section: This article was submitted to Cellular Neurophysiology, a section of the journal
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