Antibodies to morphine as indicators of chronic morphine intoxication and impaired immune reactivity.

Chronic morphine treatment of rats for 2 and 4 weeks led to an increase in morphine-binding cells in the spleen, despite the general reduction of mononuclear cell content in the spleen and thymus. Simultaneously, serum antibodies to morphine (AbM) in haemagglutination titres 1:20 and higher appeared in 50% and 80% of animals, respectively. Animals with high titres of AbM had much weaker immune response to a thymus-dependent antigen (sheep red blood cells).

[Effect of active immunization with dopamine- and norepinephrine-protein conjugated on neurochemical and neurophysiologic parameters of withdrawal syndrome in chronically morphine-treated rats].

The impact of induction of antibodies to the catecholamines (CA) dopamine (DA) and norepinephrine (NE) during active immunization of rats with CA conjugated to protein (BSA) on morphine dependence, withdrawal syndrome, and neurotransmitter status was studied during 14-day morphine treatment. DA-BSA and NE-BSA immunization of rats provided lower plasma DA concentrations in naloxone-precipitated opiate withdrawal. However, it failed to lead to normalization of hypothalamic DA levels and exacerbated the withdrawal syndrome.

[Induction of autoantibodies to serotonin and catecholamines in chronically morphine addicted rats with manifestations of abstinence syndrome].

The possibility of formation of autoantibodies to neurotransmitters has been studied in experimental model of opiate addiction. Chronic treatment of rats with morphine that leads to formation of dependence, causes induction of antibodies to norepinephrine, dopamine and serotonin. The latter could be considered as indicators of impaired neurotransmitter metabolism.