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CXCR3-dependent microglial recruitment is essential for dendrite loss after brain lesion

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Item Type:Article
Title:CXCR3-dependent microglial recruitment is essential for dendrite loss after brain lesion
Creators Name:Rappert, A. and Bechmann, I. and Pivneva, T. and Mahlo, J. and Biber, K. and Nolte, C. and Kovac, A.D. and Gerard, C. and Boddeke, H.W. and Nitsch, R. and Kettenmann, H.
Abstract:Microglia are the resident macrophage population of the CNS and are considered its major immunocompetent elements. They are activated by any type of brain pathology and can migrate to the lesion site. The chemokine CXCL10 is expressed in neurons in response to brain injury and is a signaling candidate for activating microglia and directing them to the lesion site. We recently identified CXCR3, the corresponding receptor for CXCL10, in microglia and demonstrated that this receptor system controls microglial migration. We have now tested the impact of CXCR3 signaling on cellular responses after entorhinal cortex lesion. In wild-type mice, microglia migrate within the first 3 d after lesion into the zone of axonal degeneration, where 8 d after lesion denervated dendrites of interneurons are subsequently lost. In contrast, the recruitment of microglia was impaired in CXCR3 knock-out mice, and, strikingly, denervated distal dendrites were maintained in zones of axonal degeneration. No differences between wild-type and knock-out mice were observed after facial nerve axotomy, as a lesion model for assessing microglial proliferation. This shows that CXCR3 signaling is crucial in microglia recruitment but not proliferation, and this recruitment is an essential element for neuronal reorganization.
Keywords:Microglia, Migration, Chemokine, Receptor, CXCL10, CXCR3, Dendritic Loss, Entorhinal Cortex Lesion, Facial Nerve Lesion, Animals, Mice
Source:Journal of Neuroscience
Publisher:Society for Neuroscience
Page Range:8500-8509
Date:29 September 2004
Additional Information:Copyright (c) 2004 by The Society for Neuroscience
Official Publication:https://doi.org/10.1523/JNEUROSCI.2451-04.2004
PubMed:View item in PubMed

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