Modulation of the immune response by changing neuromediator systems activity under stress.

The possible correction of the immune response affecting the mechanisms of neuroimmunomodulation in the animal model of immobilization stress is considered. Immobilization (3 h on the back) of CBA mice caused a suppression of the immune response. The number of plaque-forming cell (PFC) on the 4th day as well as rosette-forming cell (RFC) number on the 5th day of the immune reaction to sheep red blood cells (SRBC) were found to be reduced as compared to the control. Immunoinhibition in the stressed mice was reversed by the depletion of the cerebral serotonin (5-HT) with p-chlorophenylalanine (PCPA) 2 days before immobilization at a dose of 500 mg/kg. Activation of postsynaptic D-1 and D-2 dopamine (DA) receptors with apomorphine administered 30 min before stress attenuated stress-induced immunosuppression as well. Thus, the immunosuppression elicited by a stressor can be modified by drugs influencing the 5-HT and DAergic systems. It is suggested that the stress-provoked alterations of the immune response can be a consequence of changing neurochemical pattern of the brain and the disturbances of the mechanisms of psychoneuroimunomodulation.