Changes in the ultrastructure of the rat cerebral cortex after oral doses of manganese chloride.

Abstract

show progressive extrapyramidal syndrome, mental disturbances and other symptoms which are very similar to those of Parkinson’s disease [5, 7, 10, 14, 18, 19]. At the initial stages of poisoning, the neurological defect is so severe that it hides pre-existing psychopathology, which subsequently becomes clearer. The progression of these disturbances leads to the formation of stable memory and intellectual deficiency [1]. Thus, experimental models of manganese poisoning are often used for characterizing the behavioral, cellular, and molecular mechanisms of Parkinson’s disease. It is well known that in manganese neurointoxication, the highest manganese accumulation levels are seen in the basal ganglia and substantia nigra. Thus, these brain formations are the most vulnerable – degeneration of neurons and interneuronal contacts forming the nigrostriatal dopaminergic system occurs in these sites in manganese poisoning. Along with these formations, manganese also accumulates, with associated structural-functional changes, in other parts of the brain, especially the cerebral cortex [6, 8, 9, 11–13, 16, 17]. Studies of the CNS during exposure to manganese ions have mainly involved chronic poisoning with high doses and there are only a few reports of studies of the early effects [8, 17, 20]. Most morphological investigations in this area have been at the light microscope level. Thus, the aim of the present work was to study the ultrastructural changes in the rat cerebral cortex occurring during short-term poisoning with manganese chloride.