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      Methamphetamine binge administration dose‐dependently enhanced negative affect and voluntary drug consumption in rats following prolonged withdrawal: role of hippocampal FADD

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      https://www.riss.kr/link?id=O113301485

      • 저자
      • 발행기관
      • 학술지명
      • 권호사항
      • 발행연도

        2019년

      • 작성언어

        -

      • Print ISSN

        1355-6215

      • Online ISSN

        1369-1600

      • 등재정보

        SCIE;SCOPUS

      • 자료형태

        학술저널

      • 수록면

        239-250   [※수록면이 p5 이하이면, Review, Columns, Editor's Note, Abstract 등일 경우가 있습니다.]

      • 구독기관
        • 전북대학교 중앙도서관  
        • 성균관대학교 중앙학술정보관  
        • 부산대학교 중앙도서관  
        • 전남대학교 중앙도서관  
        • 제주대학교 중앙도서관  
        • 중앙대학교 서울캠퍼스 중앙도서관  
        • 인천대학교 학산도서관  
        • 숙명여자대학교 중앙도서관  
        • 서강대학교 로욜라중앙도서관  
        • 계명대학교 동산도서관  
        • 충남대학교 중앙도서관  
        • 한양대학교 백남학술정보관  
        • 이화여자대학교 중앙도서관  
        • 고려대학교 도서관  
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      다국어 초록 (Multilingual Abstract)

      While prior studies have established various interacting mechanisms and neural consequences (i.e. monoaminergic nerve terminal damage) that might contribute to the adverse effects caused by methamphetamine administration, the precise mechanisms that m...

      While prior studies have established various interacting mechanisms and neural consequences (i.e. monoaminergic nerve terminal damage) that might contribute to the adverse effects caused by methamphetamine administration, the precise mechanisms that mediate relapse during withdrawal remain unknown. This study evaluated the long‐term consequences of binge methamphetamine administration (three pulses/day, every 3 hours, 4 days, i.p.; dose–response: 2.5, 5 and 7.5 mg/kg) in adult Sprague–Dawley rats at two behavioral levels following 25 days of withdrawal: (1) negative affect (behavioral despair—forced‐swim test, and anhedonia—1% sucrose consumption, two‐bottle choice test) and (2) voluntary methamphetamine consumption (20 mg/l, two‐bottle choice test). Striatal and hippocampal brain samples were dissected to quantify monoamines content by high‐performance liquid chromatography and to evaluate neurotoxicity (dopaminergic and serotonergic markers) and neuroplasticity markers [i.e. cell fate regulator (Fas‐associated protein with death domain) FADD] by Western blot. The results showed that methamphetamine administration induced dose‐dependent negative effects during prolonged withdrawal in adult rats. In particular, rats treated repeatedly with methamphetamine (7.5 mg/kg) showed (1) enhanced negative affect—increased anhedonia associated with behavioral despair, (2) increased voluntary methamphetamine consumption, (3) enhanced neurotoxicity—decreased dopamine and metabolites in striatum and decreased serotonin in hippocampus, (4) altered neuroplasticity markers—decreased FADD protein and increased p‐FADD/FADD balance selectively in hippocampus and (5) higher consumption rates of methamphetamine that were associated with lower FADD content in hippocampus. These results confirm that methamphetamine withdrawal dose‐dependently induced negative affect and decreased monoamines content, while also increased voluntary methamphetamine consumption and suggested a role for hippocampal FADD neuroplasticity in these drug‐withdrawal adaptations.
      Methamphetamine administration induced dose‐dependent negative effects during prolonged withdrawal in adult rats. Mainly, rats treated repeatedly with methamphetamine (7.5 mg/kg) showed: (1) enhanced negative affect—increased anhedonia associated with behavioral despair, (2) increased voluntary methamphetamine consumption, (3) enhanced neurotoxicity—decreased brain dopamine and serotonin, (4) altered neuroplasticity—decreased hippocampal FADD protein, and (5) higher consumption rates of methamphetamine were associated with lower hippocampal FADD content. Thus, these results suggested a role for hippocampal FADD neuroplasticity in these drug‐withdrawal adaptations.

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