Analysis on cellular and molecular mechanism behind the depressive behavior by approaching the functional interaction between stress hormone and BDNF.

2015 Fiscal Year Final Research Report

• Project/Area Number: 24300139
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Partial Multi-year Fund
• Section: 一般
• Research Field: Neurochemistry/Neuropharmacology
• Research Institution: Kumamoto University (2014-2015); National Center of Neurology and Psychiatry (2012-2013)
• Principal Investigator: Numakawa Tadahiro 熊本大学, 発生医学研究所, 特定事業研究員 (40425690)
• Co-Investigator(Kenkyū-buntansha): CHIBA Shuichi 武蔵野大学, 付置研究所, 助教 (00510380) ; NAGATANI Miyako 聖マリアンナ医科大学, 医学部, 准教授 (20450611) ; ITAMI Chiaki 埼玉医科大学, 医学部, 講師 (90392430)
• Project Period (FY): 2012-04-01 – 2016-03-31
• Keywords: うつ病 / BDNF / グルココルチコイド / GR / ストレス

Outline of Final Research Achievements

Both increased levels of glucocorticoid concentration and dysfunction of BDNF (brain-derived neurotrophic factor) have been suggested to be involved in the onset of depressive disorder. Here, to approach the cellular and molecular mechanism behind the depressive behavior, we focused on functional crosstalk between glucocorticoid and BDNF. Using dissociated cortical neurons obtained from rat brain, we found significant influence of glucocorticoid exposure on action of BDNF, including transport of BDNF protein in neurites. Furthermore, we made transgenic mouse which expresses high levels of cortical GR, low affinity glucocorticoid receptor, to approach behavioral change under the stress, as we confirmed that GR-TrkB (BDNF receptor) interaction is important for the BDNF-mediated neurotransmission.

Free Research Field

神経科学