Changes in lymphocyte beta-adrenergic receptor density and noradrenaline content of the spleen are early indicators of immune reactivity in acute experimental allergic encephalomyelitis in the Lewis rat.

Neural activity in the spleen in the pre-clinical stage of experimental allergic encephalomyelitis (EAE) mirrored that of animals immunized with complete Freund's adjuvant (CFA) alone. In response to immune challenge the splenic noradrenaline content fell significantly, accompanied by an increase in lymphocyte beta-receptor density. The response of the pituitary-adrenal axis was reflected in increased circulating levels of corticosterone in both experimental groups; this was amplified by the stress of clinical signs leading to a 2-fold increase in animals with EAE. The increased, potentially immunosuppressive concentration of noradrenaline in the spleen during the acute stage may also represent a recovery mechanism and indicate how neuroimmune interactions could influence the relapsing-remitting nature of chronic inflammatory demyelinating disease.