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Mouse model for ablation of proliferating microglia in acute CNS injuries.

Publication Type:

Journal Article

Source:

Glia, Volume 53, Issue 3, p.331-7 (2006)

Keywords:

Animals, Antigens, CD11b, Antimetabolites, Axotomy, Brain Injuries, Cell Proliferation, Disease Models, Animal, DNA, Ganciclovir, Herpesvirus 1, Human, Hypoglossal Nerve, Immunohistochemistry, In Situ Hybridization, Mice, Mice, Transgenic, Microglia, Reverse Transcriptase Polymerase Chain Reaction, Thymidine Kinase, Wounds, Stab

Abstract:

<p>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.</p>

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