IMPAIRED NEUROGLIAL ACTIVATION IN INTERLEUKIN-6 DEFICIENT MICE

Citation
Ma. Klein et al., IMPAIRED NEUROGLIAL ACTIVATION IN INTERLEUKIN-6 DEFICIENT MICE, Glia, 19(3), 1997, pp. 227-233
Citations number
48
Categorie Soggetti
Neurosciences
Journal title
GliaACNP
ISSN journal
08941491
Volume
19
Issue
3
Year of publication
1997
Pages
227 - 233
Database
ISI
SICI code
0894-1491(1997)19:3<227:INAIID>2.0.ZU;2-M
Abstract
Astrocyte activation is a ubiquitous hallmark of the damaged brain and has been suggested to play an important regulatory role in the activa tion, survival, and regeneration of adjacent neurons, microglia, and o ligodendrocytes. Little is known, however, about the endogenous signal s that lead to this activation of astrocytes. Here we examined the reg ulation of interleukin 6 (IL6), a proinflammatory cytokine, its recept ors, and the effects of IL6-deficiency in a model of traumatic central nervous system injury in the axotomized mouse facial motor nucleus. F acial nerve transection led to a massive but transient upregulation of IL6 mRNA in the disconnected motor nucleus, while IL6-receptor subuni ts were constitutively expressed on motoneurons and astrocytes. Absenc e of IL6 in genetically IL6-deficient mice led to massive reduction in the number of activated GFAP-positive astrocytes, a more moderate dec rease in microglial activation and proliferation, and an increase in t he late neuronal response to axotomy. These results emphasize the role of ILG in the global regulation of neurons, astrocytes, and microglia and their activation in the injured nervous system. (C) 1997 Wiley-Li ss, Inc.