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Psychopharmacological Implications of Brain–Immune System Interactions

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The term antidepressant has been depicted, more than once, as a misnomer, given the wide spectrum of activity evinced by these pharmacological agents. Adding to this activity spectrum are findings that antidepressants have clear immunomodulatory effects in animals and humans. In general, antidepressants have been found to decrease immune responsiveness (Kenis and Maes 2002). Because of this, these agents may be of benefit for a wide range of symptoms that arise in the context of immune activation. Of special interest, given the ability of inflammatory cytokines to induce sickness behavior and/or major depression, a number of antidepressants have been reported to attenuate proinflammatory cytokine production, not just from peripheral immune cells (Maes 1999) but also from within the CNS, where desipramine has been reported to diminish TNF- release within the locus coeruleus (Ignatowski and Spengler 1994). Interestingly in this regard, the antidepressant efficacy of desipramine during the forced-swim test has been shown to be dependent on reductions in neuronal production of TNF- and can be reversed by exogenous TNF- coadministered with the antidepressant (Reynolds et al. 2004). Desipramine has also been shown to lower peripheral TNF- production in response to lipopolysaccharide (LPS) administration—an effect that was associated with abrogation of the depressive-like behavioral effects of LPS (Shen et al. 1999). The heterocyclic antidepressant bupropion has been similarly noted to markedly diminish TNF- production following LPS administration in animals (Brustolim et al. 2006). Of note, concomitant with attenuating proinflammatory cytokine production, antidepressants enhance production of the anti-inflammatory cytokine IL-10 (Maes et al. 1999d).

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