Effect of chronic inhalation of toluene on behavior of rats of various age groups in multi-branched maze.

The effect of a 40-day toluene inhalation on learning of young and adult rats was examined in a multi-branched maze. Experimental rats of both age groups needed more time to pass the maze and made more errors than controls. This impairment was observed in young rats immediately after termination of toluene inhalation and in adult rats immediately and 90 days after toluene.

Ultrastructure of hippocampal field CA1 in rats after status epilepticus induced by systemic administration of kainic acid.

The ultrastructure of hippocampal field CA1 in rats was studied 14 days after status epilepticus induced by administration of kainic acid. Structural changes were seen in 40% of cells, predominantly interneurons, which showed both reversible changes (mitochondria with an electron-dense matrix or small numbers of short cristae, moderate dilation of rough endoplasmic reticulum (RER) cisterns, and small numbers of ribosomes) and more significant abnormalities: swollen mitochondria with very small numbers of cristae, which were partially degraded, some with damaged mitochondrial membranes, along with pathologically damaged RER components and focal or peripheral chromatolysis. Chromatolyzed areas sometimes contained membrane-like includes and vacuoles. In addition, the neuropil contained occasional large osmiophilic formations surrounded by astrocyte processes with accumulations of glycogen or gliofibrils. Synaptoarchitectonics were also altered. Asymmetrical synapses were often seen on small dendrites and spines, with highly osmiophilic postsynaptic zones, their synaptic terminals containing numerous synaptic vesicles and large vesicles with electron-dense cores. Some presynaptic endings showed clear signs of classical dark-type degeneration. As the nucleus remained intact in all types of altered neurons, it appears that most cells underwent pathological changes of the necrotic type.

[Quantitative analysis of gliocytes and macrogliocyte-neuronal ratio in the rat hippocampus after kindling].

Gliosis is one of the main morphological correlates of epilepsy. It is presented predominantly by proliferation and hypertrophy of astrocytes and activated microglia (macrophages) and is most characteristic to those areas of the epileptogenic zones, where the loss of neurons is significant. One of such structures is the hippocampus, the sclerosis of which develops already at the early stages of epileptogenesis. Using the slides stained with cresylviolet, the quantitative analysis of gliocytes and of macrogliocyte-neuronal ratio was performed in all the areas of the hippocampus 14 and 30 days after electrical kindling. After both time intervals, the decrease of the number of neurons and the increase of the number of gliocytes were found in all the regions of the hippocampus. After 14 days the changes of gliocytes were particularly significant in the radial and oriental layers of the Ammon's horn, after 30 days they were also pronounced in CA3 pyramidal cell layer of and in hilus. Thus, hippocampal gliocytes are actively involved in the epileptogenesis.

Morphological changes and manganese content in the brains of rat pups subjected to subchronic poisoning with manganese chloride.

Morphological changes in neurons and the distributions of nerve and glial cells were studied, the glial index was calculated, and manganese (Mn) contents were determined in the caudate nucleus, the nucleus accumbens, the dorsal and ventral septal nuclei, and the frontoparietal areas of the cerebral cortex in the 40-day-old offspring of rats given different doses (10 and 20 mg/kg) of manganese chloride (MnCl2.4H2O) 15-20 days before pregnancy, during pregnancy, and for one month after parturition with the first portion of food. Mn poisoning increased Mn contents in the brains of rat pups, damaged a small proportion of neurons, and produced marked gliosis. These changes are believed to underlie previously described impairments to learning processes and emotional state in rat pups.

[Morphological changes and manganese level in the brain of rat pups subjected to subchronic manganese chloride intoxication].

The morphological alterations in the neurons together with the distribution of the neural and glial cells were studied, the glial index was calculated, and manganese level was determined in n. caudatus, n. accumbens septalis, n. dorsalis and ventralis septalis, and in the fronto-parietal region of the brain cortex in the 40-day old offspring of the rats, which were given a various daily dose (0, 10, and 20 mg/kg) of manganese chloride (MnCl2 x 4H2O) with the first portion of their food 15-20 days prior to pregnancy, during the pregnancy and for one month after the parturition. Manganese intoxication induced elevation of the manganese level in the brain of the pups with the injury of a small portions of the neurons and a pronounced gliosis. We believe that these changes underlie the previously reported disorders in learning processes and emotional state of the pups.

Kindling-induced hippocampal cell death in rats.

Quantitative analysis of the main cells and interneurons in different layers and fields of Ammon's horn, the hilus, and dentate gyrus was performed two weeks and one month after kindling, i.e., specific electrical stimulation of the ventral hippocampus. At both experimental time points, cells numbers were significantly decreased at all levels of the areas studied except the marginal layer of field CA4. Thus, in this model of experimental epilepsy, the process of epileptogenesis involved both interneurons and main cells in the hippocampus. The possible reorganization of intrahippocampal circuits and their involvement in the increased excitability characteristic of epilepsy are discussed.

[Hippocampal cell loss in rats as a result of kindling].

Quantitative analysis was performed to evaluate the numbers of principal cells cells and interneurons in differenet layers and areas of the horn of Ammonis, hilus and dentate gyrus 2 weeks and 1 month after kindling--specific electrical stimulation of ventral hippocampus. After both experimental time intervals, a significant cell loss was found in all the layers and areas studied, with the exception of stratum oriens of CA4. Thus, in this model of experimental epilepsy, both interneurons and principal cells were found to be involved in the process of epileptogenesis. Different possibilities of reorganization of intrahippocampal circuits and their participation in increased excitability, typical to epilepsy, are discussed.

[The influence of myo-inositol on the ultrastructure of hippocampal CA1 area in kainate treated rats].

The ultrastructure of neurons, synapses and astrocytes of hippocampal CA1 area in rats was investigated 14 days after: systemic injection of kainic acid and kainic acid and myo-Inositol. After injection of kainic acid numerous neurons with superficial and deep ultrastructural changes of cytoplasmic organelles were described. Among synapses numerous forms with osmiophilic active zone and single synaptic vesicles, also presynaptic terminals with core vesicles were often seen. After kainic acid + myo-Inositol injection the cells with superficial changes of organelles dominated and the synapsoarchitectonics of the area was close to normal. Thus, electrono-microscopic data indicate possible neuroprotective (antiepileptic?) features of myo-Inositol.

[Changes in the ultrastructure of neuroglia in some regions of the rat brain in manganese chloride poisoning]. / Izmeneniia ul'trastruktury neroglii nekotorykh oblastei golovnogo mozga krysy pri intoksikatsii khloristym margantsem.

Ultrastructure of astrocytes, olygodendrocytes and microgliocytes of caudate nucleus, substantia nigra and frontoparietal area of the cortex were studied under the influence of the everyday peroral treatment with MnCl2.4H2O during 30 days. Experimental animals were divided into two groups. Animals from the first group received 20 mg/kg of MnCl2.4H2O while for animals from the second one the dose made 50 mg/kg. Animals were killed on days 30 and 120 of the experiment. It was demonstrated that chloride manganese intoxication influences the ultrastructure of all types neuroglial cells, the majority of both macro- and microgliocytes remaining in normal state. Cytotoxic effect of manganese ions on astrocytes manifests in mitochondria destruction, widening of canaliculi and endoplasmic net cisterns, glycogenic granules accumulation, which leads to reduction of oxidative processes level in the nervous tissue. Increased phagocytic activity of the astrocytes was displayed in conditions of relatively high doses of MnCl2.4H2O. Microgliocyte reaction was distinctly dose-dependent and was manifested through their phagocytary activity increase. Oligodendrocytes were most stable to chloride manganese influence.

[Changes in the rat cerebral cortex ultrastructure following peroral administration of manganese chloride]. / Izmeneniia ul'trastruktury kory bol'shogo mozga krysy pri peroral'nom vvedenii khloristogo margantsa.

The effect of 30 days treatment with MnCl(2).4H2O (50 mg/kg in doze) on neuron ultrastructure and interneuronal contacts of cerebral cortex frontoparietal area was studied in rat. The material for the research was taken on 1st (group 1) and 4th (group 2) month of the experiment. Changes in neurons and cortex synapses were less significant than those in subcortical structures. In 1st group of experimental animals neurons displayed vacuolar system hyperplasia and swelling of a part of mitochondria. Changes in synapses were heterogenous from reduction of synaptic vesicles number and mitochondria swelling to degeneration after "dark" type. Despite the fact that intoxication with MnCl(2).4H2O was over, changes in cortical neurons in group 2 were significant although no cells with signs of reorganization were observed. In neuropil of rats from group 2 reduced number of synaptic vesicles as well as reorganized endings filled with amorphous osmiophilic content were encountered more often as compared to animals from group 2.