МЕТАБОЛІЗМ МЕТАЛІВ У ГІПОКАМПІ ТА РОЛЬ ЦИНКУ В ПАТОГЕНЕЗІ ЕПІЛЕПТИФОРМНИХ СУДОМ

Abstract

<p>Physiological mechanisms of convulsions status during epilepsy or episindrom significantly different from the mechanisms, which were describe for other disorders associated with glutamatergic system, such as schizophrenia (a decrease of glutamate in neurons and increased dopaminergic load), drug addiction and alcoholism (the formation of endogenous opioids and dopamine, strengthening the role of GABA-ergic system).</p><p>With glutamatergic transmission are сconnect not only convulsive state, but also the realization of higher integrative functions. Therefore, the development of epilepsy, particularly  which caused glutamate, implemented by activating Zn-ergic hippocampal neurons, associate with complex changes in human mental functions. Based on a scientific literature about  of the role of chelating zinc in the mechanisms of glutamatergic transmission, we can  suggest it participation in the mechanisms of formation of epilepsy  convulsions.</p><p>In experience on animals, was show that in the animal organism of stressing correlative changes observe zinc content and secretory material in the hippocampus, Paneth cells  and B cells of pancreas. The nature of the changes depend on the stressor. When this change of zinc content in the hippocampus and hypothalamus (as the main regulator of stress reaction) were multidirectional that this can be explained by the release of metal together with secretory material in the hypothalamus into the bloodstream. Research epileptic activity  of hippocampus by administering to the animal chelate 8 BSQ allowed to establish the dependence between convulsant action  and first  stress condition of the animal. Evocation of stress by 8-BSQ and physical activity, immobilization and alcohol abuse found that the convulsive effect of this reagent during intravitreal research increased in the case of prior exposure by specified kinds of stressors. In this pre-convulsive effect on exertion increased by 266% and the zinc content was increased by 75%; in the case of pre-immobilization duration of seizures increased by 206% and the zinc content - 50%; in the case of pre-alcoholization duration of seizures increased by 234%, and a chelating zinc content - 75%. These results suggest a chelating zinc epileptiform participate in the mechanisms of seizures and, possibly, the development of mechanisms of temporal lobe epilepsy (hippocampal). The results of studies of zinc changes in central and peripheral organs of zinc-containing simulated at different functional states allow us to make the assumption that there is a common mechanism for coordination of functional activity as the hippocampus and other zinc-containing bodies with the help of changes in the chelating zinc metabolism, regulation is carried out by means of the hippocampus.</p>