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Updated: May 10, 2026

Evaluation of Synaptic Multiplicity Using Whole-cell Patch-clamp Electrophysiology
Published on: April 23, 2019
Neuroimmune regulation of homeostatic synaptic plasticity
Horia Pribiag1, David Stellwagen1
1Centre for Research in Neuroscience, Research Institute of the McGill University Health Center, Montreal General Hospital, L7-132, 1650 Cedar Av, Montreal, QC H3G 1A4, Canada.
Abstract:
Homeostatic synaptic plasticity refers to a set of negative-feedback mechanisms that are used by neurons to maintain activity within a functional range. While it is becoming increasingly clear that homeostatic regulation of synapse function is a key principle in the nervous system, the molecular details of this regulation are only beginning to be uncovered. Recent evidence implicates molecules classically associated with the peripheral immune system in the modulation of homeostatic synaptic plasticity. In particular, the pro-inflammatory cytokine TNFα, class I major histocompatibility complex, and neuronal pentraxin 2 are essential in the regulation of the compensatory synaptic response that occurs in response to prolonged neuronal inactivity. This review will present and discuss current evidence implicating neuroimmune molecules in the homeostatic regulation of synapse function. This article is part of the Special Issue entitled 'Homeostatic Synaptic Plasticity'.
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