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The study has involved 30 children aged 4 to 6 with cleft lip and palate. Histomorphologic changes of soft tissues on cleft palate edges were detected; these inflammatory dystrophic changes are associated with reduction of the body nonspecific reactivity.

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A corrective effect of Nicotinamide on oxidation processes in ganglion and neuroglial cells of cerebral cortex sensorimotor zone in "kindling" phenomenon was studied in the experiments on mice of C57BL line. The kindling was caused by daily injection of Corazol in a dose of 30 micrograms/kg intraperitoneally during one month. The experimental mice were introduced Corazol by the same scheme but beginning from the 4th week Nicotinamide was injected daily/5, 50, 200 mg/kg intraperitoneally/30 min before Corazol introduction. Cytophotometric investigations of enzyme activity/glytamate-, succinate-, -glycerophosphate, glucose-6-phosphate-dehydrogenase and NADH-tetrazol reductase/showed that the most optimum dose of nicotinamide stimulating the tissue oxidation in the dose of 50 mg/kg. It was also established that nicotinamide in the dose of 50 mg/kg has a definite antispasmodic effect and increases ganglion cells stability to destructive effect of epiphogenic factors.

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The activity of glutamate, succinate, malate and lactate dehydrogenases in neuronal and glial hippocampal cells during corazol kindling has been cytophotometrically assessed in the experiments on (CBA X C57BL/6)F1 mice. The kindling was induced by regular intraperitoneal corazol injections in subliminal dose of 30 mg/kg. Histochemical investigations were performed 30 min, 24 hours and 30 days after the corazol injections were discontinued. The changes in the enzymatic activity revealed suggest the biphasic nature of the disturbances in energy metabolism. During the first phase (24 hours after the last injection) the enzymatic changes do not have a noticeable influence on the predominant aerobic type of oxidation. In the second phase (30 days after the last injection) lactate dehydrogenase activity significantly increases, while the activity of other enzymes under study reduces.

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Tetrapeptide tuftsin action on the activity of succinate dehydrogenase (SDG), malate dehydrogenase (MDG) and monoamine-oxidase (MAO) in microstructures of the neocortex, hippocampus and hypothalamus (supraoptic and paraventricular nuclei, retrochiasmic zone) has been investigated by means of histochemical methods. Simultaneously, pyruvate-, malate-, glutamate-, alfaketoglutamate-, succinate- and lactate-dehydrogenase activity in the neocortex and in the structures of the limbic system has been studied biochemically. SDG and MDG activity increases in neurons and glycocytes of all the hypothalamic formations mentioned. Changes in the activity of dehydrogenases in the hippocampus and neocortex under the same stimulation are less pronounced. MAO activity also increases in the nerve terminals converging on the bodies and dendrites of hypothalamic neurons and in the preterminal fibers of the neocortex, Tuftsin increases oxidative-reducing processes in various structures of the brain, but at the same time it possesses a predominant influence on the limbic system structures.

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The experiments on (CBA X C57BL/6)F1 mice have shown that regular corazol injections in subliminal doses stimulated seizure susceptibility (pharmacological kindling). Cytophotometric assay of the activity of oxidative metabolism enzymes (glutamate dehydrogenase, malate dehydrogenase, succinate dehydrogenase, alpha-oxoglutarate dehydrogenase, lactate dehydrogenase) and GABA-transaminase in the sensorimotor cortex of kindled mice in post-convulsive period, and 24 hours or 30 days after corazol injections were discontinued, has revealed some specific alterations of the enzymes under study, that suggest the existence of two phases of energy metabolism disturbances. The first phase (24 hours after corazol injections were discontinued) is characterized by intensified succinic acid oxidation, while the second phase (30 days after the last injection) is characterized by anaerobic glycolysis in neuronal and glial cells. Inhibition of GABA-transaminase activity was particularly marked in postconvulsive period. From a molecular point of view these data may be considered as enzyme disturbances during stimulation of seizure susceptability or seizure activity and as a compensation component ensuring anticonvulsive mechanisms and reparative processes (antagonistic principle of molecular mechanism regulation) during activation of antiepileptic system.

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Experiments were carried out on random-bred white rats (250-350 g). Kindling was induced by daily intraperitoneal corazol injections in subthreshold (subconvulsive) doses (30 mg/kg). It has been demonstrated that bilateral hippocampal destruction did not change the seizure threshold, while bilateral caudate nucleus destruction lowered it. Hippocampal destruction delayed corazol kindling development and also accelerated the lowering of seizure susceptibility after corazol injections were discontinued, as compared to control animals. Caudate nucleus destruction induced more marked seizure reactions in the first 14 days after corazol injections were started. There were no significant differences in seizure manifestation severity in kindled and control groups. These data point to an essential role of caudate nucleus as an element of antiepileptic system and support the concept that hippocampus plays a role of pathologic determinant which is associated with the formation of an epileptic system underlying corazol kindling.

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It has been demonstrated in (CBA X C57BL/6) F1 mice that daily corazole injections (30 mg/kg) lead to the development of pharmacological kindling that manifests in a progressive increase of seizure susceptibility, seizure occurrence in response to the subthreshold convulsant dose and in demonstrable seizures. Cytophotometric study of the histological specimens of the sensorimotor cortex discovered the reduced enzymatic activity of glutamate dehydrogenase and GABA transaminase in the neurons. In the neuroglial cells, the activity of glutamate dehydrogenase also declined, whereas that of GABA transaminase tended on the contrary, towards increase.

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The correlation between electrophysiological changes and isozymes of LDH of the rat brain cortex was studied in seizure foci induced by application of sodium penicillin. It was discovered that activity of LDH1 was suppressed, and that of LDH5 fraction was elevated in the determinant focus, which indicates the enhanced glucose anaerobic transformation. The spectrum of LDH isozymes did not practically differ from the indicators in control animals in a homotopic region of the contralateral hemisphere prior to creation of the mirror focus. The anaerobic processes were found to be increased in the mirror focus and in the determinant one as well. Similar pattern of changes in electrophysiological and neurochemical characteristics in the determinant and dependent mirror foci attests to the formation of a pathological system out of the two epileptic foci.

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