Influence of SAMe on the modifications of brain polyamine levels in an animal model of depression
Genedani S, Saltini S, Benelli A, Filaferro M, Bertolini A.
Department of Biomedical Sciences,
Section of Pharmacology,
University of Modena and Reggio Emilia,
Via G. Campi 287, 41100 Modena, Italy.
Neuroreport 2001 Dec 21;12(18):3939-3942


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.

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