Delayed onset of experimental allergic neuritis in rats treated with reserpine.

In delayed-type hypersensitivity most of the invading cells are not specifically sensitized against the initiating antigen but are augmenting cells called in by inflammatory mediators. It has been suggested that vasoactive amines, such as the monoamine serotonin, released by the action of sensitized T-cells on mast cells, may participate in the perivascular emigration of these cells that do not normally leave the blood. To test this hypothesis in experimental allergic neuritis (EAN), Lewis rats sensitized on day zero were treated with a single dose of the monoamine-depleting drug reserpine (2.5 mg/kg) immediately before the onset of early clinical signs on day nine (reserpine day 9, Rd9); during the onset of early clinical signs on day ten (Rd10); or immediately after the onset of early clinical signs on day 11 (Rd11). The results showed that the onset of early clinical signs was delayed in the Rd9 treated rats until approximately day thirteen whereas no effect on the course of the disease was observed in the Rd11 rats, and variable results were obtained in the Rd10 animals. Infiltration of mononuclear cells and leakage of 125I-albumin into the peripheral nerve was reduced in the Rd9 rats killed during the suppressed period. The delay in the onset of early clinical signs in the Rd9 rats correlated well with the time-course of serotonin depletion as reflected by levels in the peripheral blood of reserpine-treated normal animals. Although a role for histamine could not be demonstrated, the results suggest that other vasoactive amines are involved in the reaction. These results, therefore, would support the hypothesis that vasoactive amines play a role in the perivascular transit of inflammatory cells in EAN.