Analysis of changes in the serotonin inactivation coeffi cient in brain structures with simultaneous modeling of chronic neurogenic pain and malignant neoplasia

Introduction. Chronic pain syndrome in the development of malignant neoplasms has a complex polyethological character. The study of the pathogenetic mechanisms of pain during the growth of the transplanted tumor in the experiment can open up broad perspectives for the creation of new domestic analgesic drugs for use in oncology. Aim: To study the serotonin inactivation coeffi cient (SIC), the ratio of serotonin (S) and its main metabolite 5-hydroxyindolacetic acid (S-OH) in brain areas (cortex, hypothalamus) with simultaneous modeling of chronic neurogenic pain and malignant neoplasia. Material and Methods. The study involved white mongrel rats (males). To create a model of chronic pain (CP), ligation of the sciatic nerve was performed according to the method of V.V. Kravtsova in modifi cation. Rat sarcoma M-1 was used to simulate malignant neoplasia. At the main stage of the study, the animals were divided into 4 groups: control, two comparison groups (model of chronic pain, standard M-1 sarcoma grafting) and experimental (combined modeling of CP and oncological process). Animals of the second, third and fourth groups were euthanized sequentially at the 2nd and 3rd weeks of the development of the tumor process. Results. Chronic pain syndrome disrupts the process of serotonin metabolism: the decrease in SIC in the cerebral cortex of experimental animals was more signifi cant by 48% (day 14) and 72% (day 21). The development of the oncological process in comparison groups (groups 3a and 3b) is accompanied by a decrease in the level of SIC, more signifi cant at the 21th day of M-1 sarcoma development: by 37% in the hypothalamus, by 41% in the cerebral cortex. With simultaneous modeling of chronic neurogenic pain and malignant neoplasia, the lowest values of the studied indicator were noted, the decrease was 75% in the cerebral cortex (group 4a) and 87% (group 4b). Discussion. Chronic neurogenic pain and M-1 sarcoma development in isolated modeling variants cause a signifi cant decrease in SIC in hypothalamus and cerebral cortex due to disorders of serotonin formation. A more signifi cant disruption of the serotonin mediator system was noted in cerebral cortex which leads to a decrease in the body’s adaptive capabilities to pain and a disruption of the regulatory mechanisms of metabolism. Conclusion. Modifi cation of serotonin metabolism can be considered as a potential therapeutic target for the treatment of chronic pain syndrome in oncology.