Functional consequences of glia-neuron interactions in degenerating and regenerating neurons

2015 Fiscal Year Final Research Report

• Project Area: Brain Environment
• Project/Area Number: 23111007
• Research Category: Grant-in-Aid for Scientific Research on Innovative Areas (Research in a proposed research area)
• Allocation Type: Single-year Grants
• Review Section: Biological Sciences
• Research Institution: Nagoya University
• Principal Investigator: Kiyama HIroshi 名古屋大学, 医学(系)研究科(研究院), 教授 (00192021)
• Co-Investigator(Kenkyū-buntansha): KIRYU Sumiko 名古屋大学, 大学院医学系研究科, 准教授 (70311529) ; KONISHI Hiroyuki 名古屋大学, 大学院医学系研究科, 助教 (90448746)
• Project Period (FY): 2011-04-01 – 2016-03-31
• Keywords: 神経損傷 / 運動ニューロン / グリア / ATF3 / DINE / 軸索再生

Outline of Final Research Achievements

A disruption of intercellular communications among glial cells and neuron after nerve injury leads to neuronal death. We have examined molecules, which mediate interactions between glial cells and injured neurons. We have identified that DINE (damage induced neuronal endopeptidase) and PAP-III/RegIII-g (an inflammatory associated lectin-like protein) are implicated in neuron-Schwann cell interactions during nerve regeneration and development. In addition we have proved that DAP12, which is expressed by microglia, prolongs inflammatory response and is a exacerbating signal for injured motor neurons. We also succeeded in making BAC transgenic mouse Tg(ATF3-mtGPF/Cre), which expresses Cre and mitochondria localizing GFP under ATF3 promoter. This could be a useful tool for future analysis in our project as well as collaborations with other members in A01, A02 and A03.

Free Research Field

神経解剖学