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首页> 外文期刊>Addiction biology >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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Methamphetamine binge administration dose-dependently enhanced negative affect and voluntary drug consumption in rats following prolonged withdrawal: role of hippocampal FADD

机译：在延长戒断后，大鼠甲基苯丙胺静脉静脉剂剂量依赖性地增强了大鼠的负面影响和自愿药物消耗：海马FADD的作用

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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.
机译：虽然现有研究建立了各种相互作用机制和神经后果（即单氨基能神经末端损伤），其可能有助于甲基苯丙胺给药引起的不良反应，在撤回期间介导复发的确切机制仍然未知。该研究评估了在两种行为水平的成人Sprague-Dawley大鼠中的泪味甲基苯丙胺给药（三个脉冲/日，每3小时，每3小时，每3小时，4天）的长期后果在退出25天以下：（1）负面影响（行为绝望游泳试验和厌氧-1％蔗糖消费，双瓶选择试验）和（2）自愿甲基苯丙胺消费（20 mg / L，双瓶选择测试）。解离纹状体和海马脑样品以通过高效液相色谱法定量单胺含量，并评估神经毒性（多巴胺能和血清组织能标记物）和神经塑性标记物[即细胞命运调节剂（Fas-相关蛋白质，死亡域）FADD]通过Western印迹。结果表明，甲基苯丙胺给药在成年大鼠延长戒断期间诱导剂量依赖性的阴性效应。特别地，用甲基苯丙胺（7.5mg / kg）反复治疗的大鼠（1）增强了与行为绝望相关的厌氧增加的厌氧增加，（2）增加自愿甲基苯丙胺消费，（3）增强神经毒性降低的多巴胺和纹状体代谢物在海马中减少血清素，（4）改变的神经塑性标记物降低的FADD蛋白，并在海马中选择性地增加了P-FADD / FADD平衡，（5）与海马较低的甲基甲基甲基甲基甲基甲基甲基甲酸浓度增加。这些结果证实，甲基苯丙胺戒断剂量依赖性诱导的负面影响和单胺含量下降，同时也增加了自愿甲基苯丙胺消耗，并提出了对这些药物抽毒适应的海马FADD神经塑性的作用。

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