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Dematuration in the adult brain

開催日 2014/9/12
時間 15:00 - 17:00
会場 Room D(503)
Chairperson(s) 小林 克典 / Katsunori Kobayashi (日本医科大学大学院医学研究科薬理学分野 / Department of Pharmacology, Nippon Medical School, Japan)
宮川 剛 / Tsuyoshi Miyakawa (藤田保健衛生大学 総合医科学研究所 システム医科学研究部門 / Division of Systems Medical Science, Institute for Comprehensive Medical Science, Fujita Health University, Japan)

Wiring and Unwiring the Brain: Role of Glia and the Classical Complement Cascade

  • S2-D-1-2
  • Beth Stevens:1 Dorothy P Schafer:1 Ryuta Koyama:1 Yuwen Wu:1 Emily Lehrman:1 Allison P Bialas:1 Soyon Hong:1 Arnaud Frouin:1 Chris Heller:1 
  • 1:F.M. Kirby Neurobiology Center, Children's Hospital Boston, and Program in Neuroscience, Harvard Medical School, USA 

Over the past decade, it has become increasingly clear that immune molecules and cells play important roles in the development and function of the healthy nervous system. Our recent work has demonstrated that microglia, the resident CNS immune cell and phagocyte, are critical mediators of developmental synaptic pruning. Using the mouse visual system as a model, we determined that microglia engulf developing presynaptic terminals in a manner dependent upon the classical complement cascade. Furthermore, disrupting this signaling pathway resulted in significant deficits in synaptic pruning which were sustained into adulthood. We have since extended these findings to demonstrate that microglia-mediated engulfment of synapses is regulated by neural activity. Following manipulation of activity, we found that microglia preferentially engulf 'weaker' presynaptic terminals. Our data support a model by which microglia are active participants in the pruning process by selectively engulfing intact synapses destined for elimination. Using a novel synaptic competition assay, we have identified molecular mechanisms underlying activity-dependent synapse elimination. Together our findings suggest that microglia-specific and immune-related molecular pathways are regulated by neuronal activity and may be important contributors to the sculpting of neural circuits. Our findings have important implications for understanding mechanisms underlying synaptic dysfunction in autism, Rett Syndrome and other brain disorders.

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