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Mouse model for ablation of proliferating microgliain acute CNS injuries

✍ Scribed by Geneviève Gowing; Luc Vallières; Jean-Pierre Julien


Publisher
John Wiley and Sons
Year
2005
Tongue
English
Weight
258 KB
Volume
53
Category
Article
ISSN
0894-1491

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✦ Synopsis


Abstract

Activation of microglia, the primary immune effectors of the CNS and proinflammatory signaling, is a hallmark of brain damage. However, it remains controversial whether microglial cells have beneficial or detrimental functions in various neuropathological conditions. We report the generation of transgenic mice that express a mutant form of herpes simplex virus type 1 thymidine kinase (HSV‐1 TK^mt‐30^) driven by the myeloid‐specific CD11b promoter. Using two paradigms of nervous system damage, hypoglossal nerve axotomy, and cortical stab injury, we show that specific ablation of proliferating microglia in CD11b‐TK^mt‐30^ mice can be achieved by administration of ganciclovir. For example, after hypoglossal nerve injury, a 75% reduction in proliferating microglial cells was observed at the site of injury. The CD11b‐TK^mt‐30^ transgenic mouse should provide a valuable tool for studying the role of microglia in CNS damage and repair. © 2005 Wiley‐Liss, Inc.