Abstract
Depression is a biological entity consisting of psychiatric and somatic symptoms. Such symptoms are based on homeostatic dysregulation. Recently, imuune function in depression has been noted with the advance of psychoneuroimmunology. Several reports indicated depression to be accompanied by reduced immune function including reduced natural killer cell activity and lymphocyte proliferation to mitogens. On the other hand, antidepressants have been shown to suppress immune function. More attention to immunomodulation is thus needed in therapy for depression with antidepressants. Immunosuppressinve effects of antidepressants were evaluated only in vivo. Such a direct action may represent nonspedific toxic effets because of non-physiological high concentration used in the experiments. Indirect effects of antidepressants on immunity through neuroendocrine modulation should be assesed in the future to study immunomodulation by antidepressants treatment. We confirmed our previous finding indicating olfactory bulbectomy to suppress plaque forming cell (PFC) preduction to sheep red blood cells. In our recent study, immunomodulatory effects of imipramine (IMP) were evaluated by IMP administration at 5mg/kg/day for 3 or 10 days in sham-operated or olfactory bulbectomized mice. Five mg/kg/day is the physiological dose. IMP administration for 3 days caused significant suppression of PFC production in sham-operated mice and to olfactory bulbectomized mice failed to have any effect. By IMP administration for 10 days, PFC production was significantly inhibited in sham-operated mice, while restored in olfactory bulbectomized mice. Present results indicate antidepressants to exert divergent effects on immune function, depending possibly on neural functioning. Antidepressants possess modulating properties for various neurotransmission mechanisms in the brain such as beta-adrenrgic receptor downregulation. In contrast to the possibility of increased function in central beta-receptors, the function of lymphocyte beta-receptor has been shown to possibly decrease in depression and upregulate by the repeated administration of antidepressants. These differences between central and lymphyocyte beta-receptor function may be significanlt. The peripheral noradrenergic function may be under tonic inhibitory influence of the central noradrenergic system, and thus dysregulated central noradrenergic activity may induce sympathetic hyperactivity associated with immunosuppressive effects in depression. The restoration of immune function in depression by antidepressants may be related to peripheral beta-action adjustment.
