A novel GABA-mediated corticotropin-releasing hormone secretory mechanism in the median eminence 8

• Material Type: 博士論文
• Title: A novel GABA-mediated corticotropin-releasing hormone secretory mechanism in the median eminence
• Volume: 2 8
• Author/Editor: Kakizawa, Keisuke
• Author Heading: Kakizawa, Keisuke
• Publication, Distribution, etc.: American Association for the Advancement of Science
• Publication Date: 2016-08-17
• Publication Date (W3CDTF): 2016-08-17
• Alternative Title: 正中隆起におけるGABAを介した副腎皮質刺激ホルモン放出ホルモン分泌の新たなメカニズム
• Periodical title: Science Advances
• Degree grantor/type: 浜松医科大学
• Date Granted: 2016-11-18
• Date Granted (W3CDTF): 2016-11-18
• Dissertation Number: 甲第739号
• Degree Type: 博士（医学）
• Conferring No. (Dissertation): 13802甲第739号
• Text Language Code: eng
• Target Audience: 一般
• Note (General): doctoral; 医学系研究科; Corticotropin-releasing hormone (CRH), which is synthesized in the paraventricular nucleus (PVN) of the hypothalamus, plays an important role in the endocrine stress response. The excitability of CRH neurons is regulated by γ-aminobutyric acid (GABA)-containing neurons projecting to the PVN. We investigated the role of GABA in the regulation of CRH release. The release of CRH was impaired, accumulating in the cell bodies of CRH neurons in heterozygous GAD67-GFP (green fluorescent protein) knock-in mice (GAD67⁺/GFP), which exhibited decreased GABA content. The GABAA receptor (GABAAR) and the Na⁺-K⁺-2Cl⁻ cotransporter (NKCC1), but not the K⁺-Cl⁻ cotransporter (KCC2), were expressed in the terminals of the CRH neurons at the median eminence (ME). In contrast, CRH neuronal somata were enriched with KCC2 but not with NKCC1. Thus, intracellular Cl⁻ concentrations ([Cl⁻]i) may be increased at the terminals of CRH neurons compared with concentrations in the cell body. Moreover, GABAergic terminals projecting from the arcuate nucleus were present in close proximity to CRH-positive nerve terminals. Furthermore, a GABAAR agonist increased the intracellular calcium (Ca²⁺) levels in the CRH neuron terminals but decreased the Ca²⁺ levels in their somata. In addition, the increases in Ca²⁺ concentrations were prevented by an NKCC1 inhibitor. We propose a novel mechanism by which the excitatory action of GABA maintains a steady-state CRH release from axon terminals in the ME.
• DOI: 10.1126/sciadv.1501723; https://doi.org/10.1126/sciadv.1501723
• Persistent ID (NDL): info:ndljp/pid/10993847; https://dl.ndl.go.jp/pid/10993847
• Collection: 障害者向け資料
• Collection (Materials For Handicapped People:1): テキストデータ
• Collection (particular): 国立国会図書館デジタルコレクション > デジタル化資料 > 博士論文; https://dl.ndl.go.jp/collections/A00014
• Acquisition Basis: 博士論文（自動収集）
• Date Accepted (W3CDTF): 2017-12-04T02:02:48+09:00
• Date Created (W3CDTF): 2018-08-27
• Format (IMT): application/pdf
• Access Restrictions: 国立国会図書館内限定公開
• Service for the Digitized Contents Transmission Service: 図書館・個人送信対象外
• Availability of remote photoduplication service: 可
• Periodical Title (URI): http://hdl.handle.net/10271/3208; https://hama-med.repo.nii.ac.jp/records/3067
• Data Provider (Database): 国立国会図書館 : 国立国会図書館デジタルコレクション; https://dl.ndl.go.jp

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