The major cause of Parkinson's disease is progressive disturbance of dopaminergic neurons of the substantia nigra, as well as their nerve endings located in the striatum. Therefore, therapy aimed at slowing the death of dopaminergic neurons can be effective. In recent decades, various types of neuroprotective agents have been successfully used in the treatment of neurodegenerative diseases, after which the restoration of structural disfunctions of the CNS is accelerated. In the present study, we used bacterial melanin, the therapeutic effect of which is due to the improvement of the trophic effects of the brain tissue, inhibition of the inflammatory process and gliosis. The comparative study of morphological and functional state of the substantia nigra pars compacta in a rotenone model of Parkinson's disease and combined with introduction of bacterial melanin was carried out. For morphological and histochemical study, the method of detecting the activity of Ca2 + - dependent acid phosphatase was used. The analysis of the data obtained showed that during rotenone intoxication, neuronal death and substantia nigra depigmentation are observed, as well as sharp morphological changes in intracellular structures occur, which indicates gross metabolic and morphological disorders. With the introduction of bacterial melanin, there is a tendency to preserve the normal morphological picture of the neurons of the substantia nigra pars compacta, in comparison with the Parkinson's disease model.  Thus, bacterial melanin acts as a neuroprotective agent and has a supportive role in Parkinson's disease.  Keywords:  bacterial melanin, Parkinson's Disease, substantia nigra

Background. Distinct brain structures, in particular, the hippocampus, have a selective sensitivity to acute and chronic alcohol intoxication. Study of the pathogenesis of alcohol-related brain damage with a view to the development of methods of prevention and treatment is an urgent task. Objective. Our main interest was in elucidating the effects of the biologically active substance, such as taurine on cellular structures in the hippocampus following ethanol intoxication. Methods. We applied a histochemical method to estimate the Ca2 +-dependent acid phosphatase activity. The present study was carried out in female albino rats. All experimental animals received an ethanol (15%) diet as their sole source of fluid at various time points. To study the effect of taurine on cellular structures of the rat brain following short-term and chronic alcohol consumption, rats were given daily injections of taurine solution for 7 days. Results. The morphological picture of the hippocampus is characterized by swelling of granular cells in the dentate gyrus that undergo chromatolysis, as well as a decrease in numerical density and a weak expression of processes of pyramidal neurons in the early stages of alcohol consumption. Degenerative changes occur in pyramidal cells in the hippocampus in the middle periods of alcohol consumption. The density of neurons is decreased; pyramidal cells lose their characteristic shape. In the conditions of long-term alcohol consumption, not only changes in the size and number of pyramidal neurons but also in the volume of the hippocampus and its regions are observed. The morphological picture of hippocampal neurons is a morphological proof of the disorders of their metabolism. In rats treated with taurine, there are positive changes in the structural properties of neurons and an increase in phosphatase activity (increased metabolism) in the hippocampus, which determines cell survival and functional recovery of irritated neurons. Conclusion. The results indicate that taurine has a neuroprotective effect on cellular structures in rat hippocampus.

Morphofunctional characteristics of the substantia nigra (SN) were compared in four groups of experimental rats: (i) control (sham-operated), (ii) animals with a rotenone model of Parkinson's disease, PD (induced by stereotaxic unilateral microinjections of 12 μg into the median forebrain bundle), (iii) rats with modeled PD treated with i.m. injections of 100 μg/kg galarmin, and (iv) similar rats but treated with i.m. injections of a small dose of cobra venom (Naja oxiana venom, 1.0 mg/k, i.e., 5% of LD50). Four weeks after rotenone injection, frontal SN sections of all animals were examined using light microscopy and a technique for detection of Ca 2+ -dependent acid phosphatase. Clear structural disorders in the SN (decreased density of neurons, negative changes in their shape, depigmentation, low activity of acid phosphatase, etc.) were observed in rats of the second group (with the PD model). Such changes were significantly less intense in rats of the third and fourth groups (those also with the PD model, but treated with course introductions of galarmin or small doses of cobra venom); the former agent (galarmin) demonstrated somewhat better neuroprotective effects.

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