HALOPERIDOL AND SPIPERONE POTENTIATE MURINE SPLENIC B-CELL PROLIFERATION

The neuroleptics haloperidol and spiperone potentiated anti-mu induced murine B-lymphocyte proliferation in vitro and lowered the threshold of anti-mu antibody needed to trigger proliferation. Because haloperid ol and spiperone are best known for actions at D-2, 5HT(2), alpha(1), and sigma (sigma) receptors, a series of agonists and antagonists of t hese receptors were tested. Dopamine and norepinephrine inhibited, and serotonin (5HT) enhanced B-cell proliferation. Spiperone opposed the suppression of proliferation by dopamine and norepinephrine. However, antagonists of D-1, D-2, D-3, D-5, 5HT(2), 5HT(1A), and alpha(1) recep tors did not mimic the effect of haloperidol and spiperone. Furthermor e, a series of a agonists failed to affect B-cell proliferation. There fore it is likely that the effects of haloperidol and spiperone are no t due to actions at known dopamine, 5HT, alpha(1), or sigma receptors. These findings indicate neuroleptics act not only in the CNS, but als o directly on B-lymphocytes of the immune system. The pharmacological site of this action is not clear at this time.