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      Control of microglial neurotoxicity by the fractalkine receptor.

      Nature neuroscience

      deficiency, Analysis of Variance, Receptors, Chemokine, pathology, metabolism, genetics, Parkinson Disease, etiology, Neurotoxicity Syndromes, drug effects, Neurons, Nerve Tissue Proteins, Motor Neuron Disease, physiology, Microglia, Microfilament Proteins, Mice, Transgenic, Mice, Inbred C57BL, Mice, administration & dosage, Lipopolysaccharides, methods, Immunohistochemistry, Green Fluorescent Proteins, Flow Cytometry, Disease Models, Animal, Cytokines, cytology, Central Nervous System, Cells, Cultured, Cell Death, Calcium-Binding Proteins, Animals

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          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.

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          Journal
          16732273
          10.1038/nn1715

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