Expression and Role of the BDNF Receptor-TrkB in Rat Adrenal Gland under Acute Immobilization Stress

• Kondo Yusuke

  Department of Oral Pathology, Kanagawa Dental College Postgraduate School Research Institute of Salivary Gland and Health Medicine, Kanagawa Dental College

• Saruta Juri

  Department of Oral Pathology, Kanagawa Dental College Postgraduate School Department of Craniofacial Growth and Development Dentistry, Division of Orthodontics, Kanagawa Dental College Research Institute of Salivary Gland and Health Medicine, Kanagawa Dental College

• To Masahiro

  Department of Oral Pathology, Kanagawa Dental College Postgraduate School Research Institute of Salivary Gland and Health Medicine, Kanagawa Dental College

• Shiiki Naoto

  Department of Oral Pathology, Kanagawa Dental College Postgraduate School Research Institute of Salivary Gland and Health Medicine, Kanagawa Dental College

• Sato Chikatoshi

  Department of Oral Pathology, Kanagawa Dental College Postgraduate School Research Institute of Salivary Gland and Health Medicine, Kanagawa Dental College

• Tsukinoki Keiichi

  Department of Oral Pathology, Kanagawa Dental College Postgraduate School Research Institute of Salivary Gland and Health Medicine, Kanagawa Dental College

抄録

We reported that plasma brain-derived neurotrophic factor (BDNF) was maximally elevated following a 60-min period of acute immobilization stress and that salivary glands were the main source of plasma BDNF under this stress condition. However, the expression pattern of the BDNF receptor, Tyrosine receptor kinase B (TrkB), under this condition has yet to be determined. We therefore investigated the effect of this stress on the expression level of TrkB in various rat organs using real-time PCR. No significant differences were found between controls and 60 min-stressed rats with respect to TrkB level in various organs. Only adrenal glands showed significantly increased TrkB mRNA levels after 60 min of stress. TrkB mRNA and protein were observed to localize in chromaffin cells. In addition, we investigated whether BDNF-TrkB interaction influences the release of stress hormones from PC12 cells, derived from chromaffin cells. Truncated receptor, TrkB-T1, was identified in PC12 cells using RT-PCR. Exposure of PC12 cells to BDNF induced the release of catecholamine. This BDNF-evoked release was totally blocked by administration of the K252a in which an inhibitor of Trk receptors. Thus, BDNF-TrkB interactions may modulate catecholamine release from adrenal chromaffin cells under acute stress conditions.<br>

収録刊行物

• Ａｃｔａ　Ｈｉｓｔｏｃｈｅｍｉｃａ　ｅｔ　Ｃｙｔｏｃｈｅｍｉｃａ

  Ａｃｔａ　Ｈｉｓｔｏｃｈｅｍｉｃａ　ｅｔ　Ｃｙｔｏｃｈｅｍｉｃａ 43 (6), 139-147, 2010

  日本組織細胞化学会

キーワード

• acute immobilization stress
• adrenal gland
• brain-derived neurotrophic factor (BDNF)
• Tyrosine receptor kinase B (TrkB)

詳細情報

• CRID: 1390001204863214592
• NII論文ID: 130000395318
• DOI: 10.1267/ahc.10027
• ISSN: 13475800
• ISSN: 00445991
• Web Site: http://www.jstage.jst.go.jp/article/ahc/43/6/43_10027/_pdf
• Web Site: https://search.jamas.or.jp/link/ui/2012013052
• 本文言語コード: en
• データソース種別:
  • JaLC
  • Crossref
  • CiNii Articles
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