Control of microglial neurotoxicity by the fractalkine receptor View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2006-07

AUTHORS

Astrid E Cardona, Erik P Pioro, Margaret E Sasse, Volodymyr Kostenko, Sandra M Cardona, Ineke M Dijkstra, DeRen Huang, Grahame Kidd, Stephen Dombrowski, RanJan Dutta, Jar-Chi Lee, Donald N Cook, Steffen Jung, Sergio A Lira, Dan R Littman, Richard M Ransohoff

ABSTRACT

Microglia, the resident inflammatory cells of the CNS, are the only CNS cells that express the fractalkine receptor (CX3CR1). Using three different in vivo models, we show that CX3CR1 deficiency dysregulates microglial responses, resulting in neurotoxicity. Following peripheral lipopolysaccharide injections, Cx3cr1-/- mice showed cell-autonomous microglial neurotoxicity. In a toxic model of Parkinson disease and a transgenic model of amyotrophic lateral sclerosis, Cx3cr1-/- mice showed more extensive neuronal cell loss than Cx3cr1+ littermate controls. Augmenting CX3CR1 signaling may protect against microglial neurotoxicity, whereas CNS penetration by pharmaceutical CX3CR1 antagonists could increase neuronal vulnerability. More... »

PAGES

917-924

References to SciGraph publications

Journal

TITLE

Nature Neuroscience

ISSUE

7

VOLUME

9

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/nn1715

DOI

http://dx.doi.org/10.1038/nn1715

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1021332650

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/16732273


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