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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Acute tryptophan depletion in C57BL/6 mice does not induce central serotonin reduction or affective behavioural changes.
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Acute tryptophan depletion in C57BL/6 mice does not induce central serotonin reduction or affective behavioural changes.

机译：C57BL / 6小鼠中的急性色氨酸耗竭不会引起中央5-羟色胺减少或情感行为改变。

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Acute tryptophan depletion is extensively used to investigate the implication of serotonin in the onset of depressive disorders. In rats, it lowers peripheral tryptophan and decreases central serotonin concentrations. We aimed to establish the rat model of acute tryptophan depletion in the mouse for potential application as serotonin challenge tool in genetic mouse models of depression. Pharmacokinetic and behavioural effects of a tryptophan-free diet were examined in Swiss and C57BL/6 mice. Peripheral amino acids were measured and central tryptophan and serotonin concentrations were compared with anxiety and depression-like behaviour in the elevated zero-maze, forced swimming test or tail suspension test. While acute tryptophan depletion resulted in a 74% reduction of the plasma ratio tryptophan to the sum of other large neutral amino acids in Swiss mice 1h after administration (2x10 ml/kg, 30 min interval), there was only a 40% reduction in C57BL/6 mice. The latter did not show anxiety in the elevated zero-maze or increased immobility in the forced swimming test or tail suspension test. A higher dose (2x20 ml/kg) with a longer interval (60 min) reduced the ratio with 68% in C57BL/6 mice, lowered hippocampal serotonin turnover and had no functional effect when tested in the elevated zero-maze and forced swimming test. These findings have important implications for the use of acute tryptophan depletion in general and in particular for its application in mice. Although in healthy mice no clear central serotonin or functional effects were observed, further research is indicated using mice with pre-existing serotonin dysfunction, as they might be more vulnerable to acute tryptophan depletion.
机译：急性色氨酸耗竭被广泛用于研究5-羟色胺在抑郁症发作中的意义。在大鼠中，它降低外周色氨酸并降低中央血清素浓度。我们旨在建立小鼠急性色氨酸耗竭的大鼠模型，以作为5-羟色胺挑战工具在抑郁症基因小鼠模型中的潜在应用。在瑞士和C57BL / 6小鼠中检查了无色氨酸饮食的药代动力学和行为效应。在升高的零迷宫，强迫游泳测试或尾巴悬吊测试中，测量了外周氨基酸，并将中枢色氨酸和5-羟色胺的浓度与焦虑和抑郁样行为进行了比较。急性色氨酸耗竭导致给药后1h（2x10 ml / kg，30分钟间隔）的瑞士小鼠血浆色氨酸与其他大中性氨基酸的总和降低74％，而C57BL仅降低40％ / 6只老鼠。后者在升高的零迷宫中没有表现出焦虑感，在强迫游泳测试或尾部悬挂测试中没有表现出不动感。在较高的零迷宫和强迫游泳试验中进行测试时，较高的剂量（2x20 ml / kg）和较长的间隔（60分钟）可使C57BL / 6小鼠的比例降低68％，降低海马血清素的转化率，并且没有功能作用。这些发现总体上对于急性色氨酸耗竭的使用具有重要意义，特别是对于其在小鼠中的应用。尽管在健康小鼠中未观察到明显的中央5-羟色胺或功能作用，但仍需进一步研究，以使用已有5-羟色胺功能障碍的小鼠，因为它们可能更容易遭受急性色氨酸耗竭。

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