Role for inducing neural plasticity of supplying of energetic substrate in injured spinal cord.

2014 Fiscal Year Final Research Report

• Project/Area Number: 25893291
• Research Category: Grant-in-Aid for Research Activity Start-up
• Allocation Type: Single-year Grants
• Research Field: Orthopaedic surgery
• Research Institution: National Rehabilitation Center for Persons with Disabilities
• Principal Investigator: ICHIHARA Yoshinori 国立障害者リハビリテーションセンター(研究所), 研究所 運動機能系障害研究部, 流動研究員 (50710711)
• Project Period (FY): 2013-08-30 – 2015-03-31
• Keywords: オリゴデンドロサイト / 髄鞘 / グルコース / グリコーゲン / 乳酸

Outline of Final Research Achievements

We examined the contribution of glycogen to remyelination as an inducible neural plasticity, which is therapeutic target of spinal cord injury. Therefore we tested the effect of inhibitor of glycogen phosphorylase, glycogen catabolic enzyme, in mice reversible demyelination model, named cuprizone model. We found that remyelination was decreased in corpus callosum of inhibitor injected mice compared to saline injected mice. To further examine the possibility whether lactate derived from glycogen affects proliferation or maturation of oligodendrocyte progenitor cells (OPCs), we cultured OPCs and tested the effect of lactate. Increased cell death, decreased OPCs proliferation and inhibited differentiation to oligodendrocyte by low glucose was rescued by lactate.
These results suggest that oligodendrocytes use metabolites derived from glycogen for remyelination in vivo and lactate might be used for proliferation and maturation in oligodendrocytes.

Free Research Field

分子生物学