期刊
NEUROREPORT
卷 12, 期 18, 页码 3939-3942出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/00001756-200112210-00017
关键词
s-adenosyl-L-methionine; antidepressants; chronic mild stress; depression; polyamines; hippocampus; nucleus accumbens; rat
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.
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