Influence of chronic administration of antiparkinson drugs on levels of serum autoantibodies to dopamine and NMDA receptors

Abstract

In experiments on 108 rats, changes in the level of serum autoantibodies to NMDA receptors (subunits NR1, NR2A, NR2B) and dopamine receptors of the first and second types (DR1 and DR2) were studied during chronic intraperitoneal administration of antipsychotics, antiparkinsonian drugs and their combination. The highest values of autoantibodies to NR1 and NR2A subunits were revealed when bromocriptine was used and to NR2B -when amantadine was administered. Chronic administration of haloperidol at a dose of 0.5 mg/kg increased serum levels of autoantibodies to NMDA receptors, especially in the NR2A subunit. At a dose of 0.1 mg/kg, haloperidol increased the content of autoantibodies to DR1 dopamine receptors. The use of an antipsychotic in combination with antiparkinsonian drugs led to an even more significant increase in the levels of autoantibodies to NR1, NR2A, DR1 and DR2, especially with the combined administration of bromocriptine and haloperidol. At the same time, haloperidol prevented the increase in autoantibodies to NR2B caused by antiparkinsonian drugs. The isolated use of haloperidol or bromocriptine, as well as their joint administration, increased the level of autoantibodies to the S100B protein in the blood serum, and amantadine eliminated this increase in autoantibodies. An increase in the concentration of autoantibodies to the S100B protein correlated with a high content of autoantibodies to NR1 and NR2A, as well as low content of NR2B.