Influence of SAMe on the modifications of brain polyamine levels in an animal model of depression
Influence of SAMe on the modifications of brain polyamine levels in an animal model of depression
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DOI：
10.1097/00001756-200112210-00017
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发表时间：
2001-12-21
期刊：
影响因子：
1.7
通讯作者：
Bertolini, A
中科院分区：
文献类型：
--
作者：
Genedani, S;Saltini, S;Bertolini, A
S-腺苷-L-甲硫氨酸（SAMe）的抗抑郁活性机制尚未阐明。 SAMe 对于多胺的合成至关重要，而多胺在蛋白质合成、细胞增殖和神经元可塑性中发挥着关键作用。另一方面，越来越多的数据表明，抑郁症与区域脑容量的减少有关，抗抑郁药会增加特定大脑区域的神经发生，并影响神经元的可塑性。在这里，我们表明，在经过验证的抑郁症大鼠模型（慢性不可预测的轻度应激诱发的快感缺失）中，海马中的腐胺、亚精胺和精胺显着减少，并且伏隔核中仅腐胺显着减少。 SAMe 在完全抗抑郁剂量下（肌肉注射 300 毫克/千克，每天 7 天），完全恢复伏隔核中腐胺的水平，并部分恢复海马中亚精胺和精胺的水平。这些结果可能表明（i）大脑多胺在抑郁和奖励过程中发挥作用； (ii) SAMe 的抗抑郁作用可能至少部分归因于伏隔核中腐胺水平的正常化。 NeuroReport 12:3939-3942 (C) 2001 Lippincott Williams & Wilkins。
The mechanism(s) of the antidepressant activity of S-adenosyl-L-methionine (SAMe) have not yet been elucidated. SAMe is essential for the synthesis of polyamines, which have a key role in protein synthesis, cell proliferation, and neuronal plasticity. On the other hand, accumulating data indicate that depression is associated with a reduction in regional brain volume and that antidepressants increase neurogenesis in defined brain regions and also influence neuronal plasticity. Here we show that in a validated rat model of depression (chronic unpredictable mild stress-induced anhedonia) there is a significant reduction of putrescine, spermidine and spermine in the hippocampus, and of only putrescine in the nucleus accumbens septi. SAMe, at a fully antidepressant dose (300 mg/kg i.m., daily for 7 days), completely restores the levels of putrescine in the nucleus accumbens, and restores in part the levels of both spermidine and spermine in the hippocampus. These results may suggest (i) a role for brain polyamines in depression and in reward processes; and (ii) that the antidepressant effect of SAMe may be due, at least in part, to a normalization of putrescine levels in the nucleus accumbens septi. NeuroReport 12:3939-3942 (C) 2001 Lippincott Williams & Wilkins.