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Varied actions of proinflammatory cytokines on excitotoxic cell death in the rat central nervous system
Author(s) -
Allan Stuart M.
Publication year - 2002
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.10142
Subject(s) - ampa receptor , proinflammatory cytokine , neuroprotection , neurodegeneration , striatum , programmed cell death , glutamate receptor , tumor necrosis factor alpha , neuroscience , central nervous system , interleukin , inflammation , biology , immunology , receptor , medicine , cytokine , apoptosis , biochemistry , disease , dopamine
Interleukin (IL)‐1β mediates diverse forms of neurodegeneration and exacerbates cell death induced by striatal injection of the excitotoxin α‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazole propionic acid (AMPA) in the rat brain. The objective of this study was to determine whether this effect was specific to IL‐1β. Injection of IL‐1α and AMPA in the striatum had effects identical to those of IL‐1β, whereas coinjection of IL‐6 or tumor necrosis factor (TNF)‐α with AMPA failed to induce significant cortical cell death. In contrast to IL‐1α, IL‐1β, and IL‐6, TNFα significantly reduced (by 38%) the local striatal damage. These findings suggest that the effect of IL‐1 on AMPA receptor‐mediated cell death in the rat striatum is not mimicked by other proinflammatory cytokines. Furthermore, TNFα shows neuroprotective effects against acute excitotoxic injury. © 2002 Wiley‐Liss, Inc.