Influence of SAMe on the modifications of brain polyamine levels in an animal model of depression.

Full Abstract

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.

Author information

Author/s: Genedani, S (S); Saltini, S (S); Benelli, A (A); Filaferro, M (M); Bertolini, A (A);

Affiliation: Department of Biomedical Sciences, Section of Pharmacology, University of Modena and Reggio Emilia, Via G. Campi 287, 41100 Modena, Italy.

Journal and publication information

Publication Type: Journal Article; Research Support, Non-U.S. Gov't

Journal: Neuroreport (Neuroreport), published in England. (Language: eng)

Reference: 2001-Dec; vol 12 (issue 18) : pp 3939-42

Dates: Created 2001/12/19; Completed 2002/03/18; Revised 2008/11/21;

PMID: 11742215, status: MEDLINE (last retrieved date: 2/18/2009)

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