The role of Cholecystokinin B receptor (CCKBR) in axonal elongation

Research Project

Project/Area Number	15K10397
Research Category	Grant-in-Aid for Scientific Research (C)
Allocation Type	Multi-year Fund
Section	一般
Research Field	Orthopaedic surgery
Research Institution	Hamamatsu University School of Medicine
Principal Investigator	Hasegawa Tomohiko 浜松医科大学, 医学部附属病院, 講師 (50402368)
Project Period (FY)	2015-04-01 – 2018-03-31
Project Status	Completed (Fiscal Year 2017)
Budget Amount *help	¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000) Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000) Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000) Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Keywords	conditioning / nerve regeneration / cckbr / dorsal root ganglion / sciatic nerve injury / 神経再生 / 再生医学
Outline of Final Research Achievements	Pre-conditioning peripheral nervous system (PNS) neurons by a peripheral axonal injury primes them through massive transcriptional changes to regenerate more vigorously and faster in the face of a second injury because of an induction of networks of regeneration-associated genes. Studies of the transcriptional response in pre-conditioned dorsal root ganglion (DRG) neurons have implicated regeneration-promoting roles for many transcription factors and regeneration-associated genes. Among them, cholecystokinin B receptor (CCKBR) gene increases ten times at DRG after pre-conditioning. However, the role of CCKBR in regeneration is yet to be elucidated. The purpose of this study is to investigate the role of CCKBR in association with peripheral nerve regeneration. In loss-of-function experiments, LY225910 significantly reduced neurite initiation (53% reduction, P＜0.001) and maximal axon length (64% reduction, P＜0.001) relative to vehicle controls.