Related Experiment Video
Updated: Jun 10, 2026

A High-content Assay for Monitoring AMPA Receptor Trafficking
Published on: January 28, 2019
AMPA-receptor trafficking and injury-induced cell death
Michael S Beattie1, Adam R Ferguson, Jacqueline C Bresnahan
1Brain and Spinal Injury Center, Department of Neurological Surgery, University of California, San Francisco, Bldg. 1, Rm 101, San Francisco, CA 94110, USA. michael.beattie@ucsf.edu
Abstract:
AMPA receptors (AMPARs) are critical for synaptic plasticity, and are subject to alterations based on subunit composition and receptor trafficking to and from the plasma membrane. One of the most potent regulators of AMPAR trafficking is the pro-inflammatory cytokine tumor necrosis factor (TNF)α, which is involved in physiological regulation of synaptic strength (Beattie et al., (2002) Science, 295, 2282-2285; Stellwagen and Malenka, (2006) Nature, 440, 1054-1059) and is also present at high concentrations after CNS injury. Here, we review evidence that TNF can rapidly alter the surface expression of AMPARs so that the proportion of Ca(++) -permeable receptors is increased and that this increase, in combination with increased levels of extracellular glutamate after injury, plays an important role in enhancing excitotoxic cell death after CNS injury. Thus, the pathophysiological hijacking of a critical regulator of synaptic plasticity and homeostasis by the secondary injury cascade may represent a new therapeutic target for neuroprotection.
More Related Videos
Related Concept Videos
Cellular Injury I: Introduction
Cellular Injury IlI: Cellular Death
Cellular Injury V: Apoptosis and Autophagy
The Extrinsic Apoptotic Pathway
Cellular Injury IV: Necrosis
Receptor Downregulation in MVBs
The EGFR can initiate signaling pathways that lead to cell proliferation, migration, and differentiation. Overexpression of EGFR stimulates cells to proliferate. Excessive EGFR activation may...

