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Interleukin-1 beta modulates AMPA receptor expression and phosphorylation in hippocampal neurons

Lai, Aaron Y., Swayze, Richard D., El-Husseini, Alaa, Song, Cai·2006·Journal of Neuroimmunology
DOI 10.1016/j.jneuroim.2006.03.001
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Abstract

Interleukin (IL)-1beta is a pro-inflammatory cytokine involved in modulating inflammation and stress responses in the brain. Central administration of IL-1beta impairs both memory functions and long-term potentiation (LTP) induction. However, the molecular events responsible for the downstream effects of IL-1beta are not fully understood. Given the potential regulatory role of IL-1beta in LTP, we assessed whether IL-1beta influences surface expression and phosphorylation of glutamate receptors. We found that IL-1beta, but not IL-10 or tumour necrosis factor (TNF)-alpha, down-regulated the surface expression and Ser831 phosphorylation of the alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor subunit GluR1. Agents that block IL-1beta receptor activity abolished these effects. In contrast, no change in the surface expression of the N-methyl-d-aspartate (NMDA) receptor subunit NR1 was observed. The inhibition of NMDA receptor activity or depletion of extracellular calcium blocked IL-1beta effects on GluR1 phosphorylation and surface expression. NMDA-mediated calcium influx was also regulated by IL-1beta. These findings suggest that IL-1beta selectively regulates AMPA receptor phosphorylation and surface expression through extracellular calcium and an unknown mechanism involving NMDA receptor activity.

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Metadata

Authors
Lai, A. Y., Swayze, R. D., El-Husseini, A., & Song, C.
Venue
Journal of Neuroimmunology
Publisher
Elsevier BV
Published
2006-06
Volume
175
Issue
1-2
Pages
97-106
ISSN
0165-5728
DOI
10.1016/j.jneuroim.2006.03.001
Cited by
151
References
5
Language
en
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