2019年04月12日　　Friday Lunch Seminar
12:15 〜 13:00

CiNet　1F　Conference Room

“慢性疼痛の分子機構：免疫から脳ネットワークリモデリング”

熊谷 雄太郎

産業技術総合研究所
生命工学領域 創薬基盤研究部門
ステムセルバイオテクノロジー研究グループ
主任研究員

担当 PI: 中江 文

Abstract:

Chronic post-surgical pain (CPSP) is a cause of pain suffering even after recovery from surgical insult with incidence rate of 5-50 %. Prior studies suggest that excessive activation of peripheral neurons as well as remodeling of neural circuit by microglia and/or astrocytes are cause of CPSP. However, its molecular mechanism is still elusive. To elucidate the mechanism of CPSP, we devised our original CPSP animal model and investigated the mice with deficiency in various genes involved in inflammatory response and migration of immune cells. We have found that mice deficient in genes involved in inflammatory response were resistant to CPSP. These results indicate that strong inflammation and migration of monocytes into the brain caused by surgical insult are essential molecular basis for CPSP. Moreover, to clarify molecular mechanism under inflammatory remodeling of the brain, we performed transcriptome analysis of whole brain of CPSP mice, and have found that expression levels of genes specific for myelinated oligodendrocytes was reduced. This indicates reduction of myelinated oligodendrocytes in the brain after onset of CPSP which resembles demyelination.