Inhibitory effects of amantadine on the production of pro-inflammatory cytokines by stimulated in vitro human blood.
Journal Title: Pharmacological Reports - Year 2009, Vol 61, Issue 6
Abstract
Treatment with amantadine (AMA), an N-methyl-D-aspartate (NMDA) receptor antagonist and antidepressant drug, increased the antidepressant activity of subsequent drugs in experimental studies and in patients suffering from treatment-resistant depression (TRD). Recent evidence indicates that depression may be accompanied by activation of an inflammatory response. These data indicate that pro-inflammatory cytokines may play a role in the etiology of depression, particularly in TRD. The present in vitro study shows the ability of AMA, used at concentrations between 10(-7) to 10(-5) M, to reduce the production of the pro-inflammatory cytokines, specifically interferon-gamma (IFN-gamma) and tumor necrosis factor-alpha (TNF-alpha). In addition, AMA treatment increased the production of the negative immunoregulator, interleukin-10 (IL-10). Furthermore, the combined treatment of AMA with fluoxetine (FLU), but not imipramine (IMI), had a stronger immunomodulatory effect on cytokine production than AMA alone. The above data provide additional rationale for the treatment of patients suffering from depression with a combination of AMA and a selective serotonin reuptake inhibitor.
Authors and Affiliations
Marta Kubera, Michael Maes, Bogusława Budziszewska, Agnieszka Basta-Kaim, Monika Leśkiewicz, Beata Grygier, Zofia Rogóż, Władysław Lasoń
Keywords
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