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      The classical complement cascade mediates CNS synapse elimination.

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          Abstract

          During development, the formation of mature neural circuits requires the selective elimination of inappropriate synaptic connections. Here we show that C1q, the initiating protein in the classical complement cascade, is expressed by postnatal neurons in response to immature astrocytes and is localized to synapses throughout the postnatal CNS and retina. Mice deficient in complement protein C1q or the downstream complement protein C3 exhibit large sustained defects in CNS synapse elimination, as shown by the failure of anatomical refinement of retinogeniculate connections and the retention of excess retinal innervation by lateral geniculate neurons. Neuronal C1q is normally downregulated in the adult CNS; however, in a mouse model of glaucoma, C1q becomes upregulated and synaptically relocalized in the adult retina early in the disease. These findings support a model in which unwanted synapses are tagged by complement for elimination and suggest that complement-mediated synapse elimination may become aberrantly reactivated in neurodegenerative disease.

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          Author and article information

          Journal
          Cell
          Cell
          Elsevier BV
          0092-8674
          0092-8674
          Dec 14 2007
          : 131
          : 6
          Affiliations
          [1 ] Department of Neurobiology, Stanford University School of Medicine, Stanford, CA 94305, USA. beths@standfordmedalumni.org
          Article
          S0092-8674(07)01355-4
          10.1016/j.cell.2007.10.036
          18083105
          cf686dda-2156-4727-ae2b-7a3e53875a9d
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