[A role of diencephalic monoaminergic dysfunction in chronic neurogenic pain].

Changes in catecholamine pool (epinephrine, norepinephrine, dopamine) and 5-oxyindoles (serotonin, 5-oxyindolacetic acid) in the diencephalic structures were studied in 2, 15, 40 days of neurogenic pain syndrome development in rats with double-sided entrapment of N. ischiadicus. The main manifestations of monoamine diencephalic dysfunction in the period of neurogenic pain chronization were described: the reduction of catecholamine pool, most evident in the thalamus; absolute and relative serotonin increase (especially in the hypothalamus); "minimization" of thalamus monoamine potential and shift of diencephalic balance to the hypothalamic MA-ergic component domination. The possible mechanisms of the imbalance and its role in the deformation of noci-antinociceptive interaction in the neurogenic pain process are discussed.

[The features of bulbo-spinal serotoninergic reaction in the young rats under the condition of acute somatic paiN].

Postnatal changes of background and stress-induced (by electric skin nociceptive irritation) concentrations of serotonin (S) and 5-oxyindolacetic acid (5-OIAA)in medulla oblongata and in spinal marrow was investigated using the male white rats (2-4, 17-18 and 30-35 days old). In the intact rats of these three groups the differences of S concentration in medulla oblongata were not revealed. S concentration in spinal marrow and 5-OIAA concentrations in both structures were changed in phase: decreased during vision-appearing period and increased during 1 month age. Rats of three groups showed the following reactions to the pain: 2-4 day rats - increase of spinal pool of S and 5-OIAA and decrease of 5-OIAA fraction in medulla oblongata; 17-18 day rats - hypo-S-shift in both structures, decrease 5-OIAA in spinal marrow and its increase in medulla oblongata; 30-35 day rats - pronounced reduction of both S and 5-OIAA at a bulbo-spinal level. Mechanisms of revealed postnatal changes of S metabolism in CNS and their role in age features of pain sensitivity formation in early ontogenesis were discussed.