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      GABA from reactive astrocytes deteriorates anxiety and aggression in adolescence period in mouse by early life stress = 발달초기 스트레스에 노출된 사춘기 생쥐에서 반응성 성상세포 유래 GABA가 불안과 공격성을 악화시킨다

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      https://www.riss.kr/link?id=T16306762

      • 저자
      • 발행사항

        Daejeon : Eulji University, 2022

      • 학위논문사항
      • 발행연도

        2022

      • 작성언어

        영어

      • KDC

        510 판사항(6)

      • DDC

        610 판사항(23)

      • 발행국(도시)

        대전

      • 형태사항

        xi, 108 leaves : illustrations (some color) ; 26 cm

      • 일반주기명

        Adviser: Sun Seek Min
        Includes bibliographies

      • 소장기관
        • 국립중앙도서관 국립중앙도서관 우편복사 서비스
        • 을지대학교 대전캠퍼스 학술정보원 소장기관정보
        • 을지대학교 의정부캠퍼스 학술정보원 소장기관정보
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      다국어 초록 (Multilingual Abstract) kakao i 다국어 번역

      Astrocyte reactivity can be stimulated by variety of sources in response to plenty of central nervous system pathologies like trauma, stroke or various neurodegenerative diseases. Normal astrocyte reactivity can protect neural tissue, maintain tissue homeostasis, and preserve neurological functions. Dysfunction of reactive astrocytes can impart to disorder of central nervous system (CNS) either through loss of normal functions or through gain of abnormal functions. The latest research show that reactive astrocytes excessively produce the inhibitory gliotransmitter gamma-aminobutyric acid (GABA) by monoamine oxidase-B (MAOB) and abnormally release GABA through the bestrophin 1 (Best1) channel. This research focuses on the properties of the GABA from glial cells and their expression in paraventricular nucleus (PVN), basolateral amygdala (BLA), central nucleus of amygdala (CeA) and dentate gyrus (DG) of ventral hippocampus that relates early life stress in maternal separation (MS) model of mouse. Many studies had been done with relation to different animal model to understand the role of GABA, its synthesis and release in the glial cells. However, there had not been much investigation in astrocytic reactivity of GABA and its expression specially on emotion disorder in the model of early life stress (ELS). Thus, this research integrated about the ELS and focus mostly on anxiety and aggression as an animal model of MS, to show how ELS affects glial cell function specially astrocytes. Specially, this study focuses on the immunoreactivity expression of GABA, MAOB and Best1 channel in three major regions of brain. Importantly, the finding also emphasizes the roles GABA in reactive astrocytes and be a potential intervention target for anxiety and aggression in ELS model in future.
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      Astrocyte reactivity can be stimulated by variety of sources in response to plenty of central nervous system pathologies like trauma, stroke or various neurodegenerative diseases. Normal astrocyte reactivity can protect neural tissue, maintain tissue ...

      Astrocyte reactivity can be stimulated by variety of sources in response to plenty of central nervous system pathologies like trauma, stroke or various neurodegenerative diseases. Normal astrocyte reactivity can protect neural tissue, maintain tissue homeostasis, and preserve neurological functions. Dysfunction of reactive astrocytes can impart to disorder of central nervous system (CNS) either through loss of normal functions or through gain of abnormal functions. The latest research show that reactive astrocytes excessively produce the inhibitory gliotransmitter gamma-aminobutyric acid (GABA) by monoamine oxidase-B (MAOB) and abnormally release GABA through the bestrophin 1 (Best1) channel. This research focuses on the properties of the GABA from glial cells and their expression in paraventricular nucleus (PVN), basolateral amygdala (BLA), central nucleus of amygdala (CeA) and dentate gyrus (DG) of ventral hippocampus that relates early life stress in maternal separation (MS) model of mouse. Many studies had been done with relation to different animal model to understand the role of GABA, its synthesis and release in the glial cells. However, there had not been much investigation in astrocytic reactivity of GABA and its expression specially on emotion disorder in the model of early life stress (ELS). Thus, this research integrated about the ELS and focus mostly on anxiety and aggression as an animal model of MS, to show how ELS affects glial cell function specially astrocytes. Specially, this study focuses on the immunoreactivity expression of GABA, MAOB and Best1 channel in three major regions of brain. Importantly, the finding also emphasizes the roles GABA in reactive astrocytes and be a potential intervention target for anxiety and aggression in ELS model in future.

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      목차 (Table of Contents)

      • Ⅰ. INTRODUCTION = 1
      • Early life stress(ELS) = 1
      • Maternal separation(MS) = 2
      • Effects of ELS on glial cells = 7
      • Glial cells = 7
      • Ⅰ. INTRODUCTION = 1
      • Early life stress(ELS) = 1
      • Maternal separation(MS) = 2
      • Effects of ELS on glial cells = 7
      • Glial cells = 7
      • Astrocytes = 9
      • Effects of MS on astrocytes = 10
      • Reactive astrocytes = 11
      • Role of reactive astrocytes and gliotransmitter = 12
      • Pathway of production and regulation of GABA in Astrocytes = 13
      • Purpose of study = 15
      • Ⅱ. MATERIALS AND METHODS = 16
      • Experimental Animal = 16
      • Maternal Separation Protocol = 17
      • Behavior test = 18
      • Open Field Test(Three Consecutive days of the) = 19
      • Elevated Plus Maze test = 20
      • Y-maze test = 21
      • Tube-dominance test = 22
      • Resident-intruder test = 23
      • Immunofluorescence = 24
      • Animal perfusion fixation = 26
      • Immunofluorescence protocol = 26
      • Fluorescent microscopy and quantification = 30
      • Ⅲ. Results = 31
      • Early life stress (MS model) group manifested anxiety-like behavior = 31
      • Early life stress (MS model) group manifested aggressive-like behavior = 34
      • Immunoreactivity and intensity of GABA in GFAP positive area in PVN = 36
      • Immunoreactivity and intensity of MAOB in GFAP positive area in PVN = 40
      • Immunoreactivity and intensity of Best1 in GFAP positive area in PVN = 43
      • Immunoreactivity and intensity of GABA in GFAP positive area in Amygdala = 46
      • Immunoreactivity and intensity of MAOB in GFAP positive area in Amygdala = 50
      • Immunoreactivity and intensity of bestrophin 1 in GFAP positive area in amygdala = 53
      • Reactive astrocytes release GABA in Ventral hippocampal of DG region = 56
      • GABA synthesis by MAOB in Ventral hippocampal of DG region = 60
      • GABA is released from reactive astrocytes via Best1 channel in Ventral hippocampal of DG region = 63
      • Ⅳ. Discussion = 66
      • GABA, MAOB and Best 1 and their function = 66
      • Behavior test = 67
      • Immunofluorescent test = 68
      • Synaptic functional plasticity? = 69
      • Potential pathway for GABA release = 70
      • Putrescine oxidation pathway = 70
      • Expression of astrocytic GABA on mice model of anxiety and aggression in paraventricular nucleus = 72
      • Expression of astrocytic GABA on mice model of anxiety and aggression in amygdala = 75
      • Expression of astrocytic GABA on mice model of anxiety and aggression in ventral hippocampus of DG (granular layer) = 76
      • Ⅴ. Conclusion = 79
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      참고문헌 (Reference)

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