• Open Access

Role of TrkB expression in rat adrenal gland during acute immobilization stress

Authors

  • Yusuke Kondo,

    1. Department of Environmental Pathology and Research Institute of Salivary Gland and Health Medicine, Graduate School of Kanagawa Dental College, Yokosuka, Japan
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  • Masahiro To,

    1. Department of Environmental Pathology and Research Institute of Salivary Gland and Health Medicine, Graduate School of Kanagawa Dental College, Yokosuka, Japan
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  • Juri Saruta,

    1. Department of Environmental Pathology and Research Institute of Salivary Gland and Health Medicine, Graduate School of Kanagawa Dental College, Yokosuka, Japan
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  • Takashi Hayashi,

    1. Department of Environmental Pathology and Research Institute of Salivary Gland and Health Medicine, Graduate School of Kanagawa Dental College, Yokosuka, Japan
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  • Hiroki Sugiyama,

    1. Department of Environmental Pathology and Research Institute of Salivary Gland and Health Medicine, Graduate School of Kanagawa Dental College, Yokosuka, Japan
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  • Keiichi Tsukinoki

    Corresponding author
    • Department of Environmental Pathology and Research Institute of Salivary Gland and Health Medicine, Graduate School of Kanagawa Dental College, Yokosuka, Japan
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Address correspondence and reprint requests to Keiichi Tsukinoki,DDS, Ph.D, Department of Environmental Pathology, Graduate School of Kanagawa Dental College, 82 Inaoka-cho, Yokosuka, Kanagawa 238-8580, Japan. E-mail: ktsukino@kdcnet.ac.jp

Abstract

Expression of tyrosine receptor kinase B (TrkB), a receptor for brain-derived neurotrophic factor (BDNF), is markedly elevated in the adrenal medulla during immobilization stress. Catecholamine release was confirmed in vitro by stimulating chromaffin cells with recombinant BDNF. We investigated the role of TrkB and the localization of BDNF in the adrenal gland during immobilization stress for 60 min. Blood catecholamine levels increased after stimulation with TrkB expressed in the adrenal medulla during 60-min stress; however, blood catecholamine levels did not increase in adrenalectomized rats. Furthermore, expression of BDNF mRNA and protein was detected in the adrenal medulla during 60-min stress. Similarly, in rats undergoing sympathetic nerve block with propranolol, BDNF mRNA and protein were detected in the adrenal medulla during 60-min stress. These results suggest that signal transduction of TrkB in the adrenal medulla evokes catecholamine release. In addition, catecholamine release was evoked by both the hypothalamic–pituitary–adrenal axis and autocrine signaling by BDNF in the adrenal gland. BDNF–TrkB interaction may play a role in a positive feedback loop in the adrenal medulla during immobilization stress.

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