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Biomedical subjects

I V Viktorov

Publications and source records attributed to I V Viktorov.

At least 19 recordsLinked to original sources
PubMed2001

Structure of cell clusters formed in cultures of dissociated human embryonic brain.

Cell clusters in a culture of dissociated brain from human fetuses at 8-12 weeks gestation in a serum-free growth medium were studied by immunohistochemical methods and electron microscopy. Heterogeneity of cell population in culture was demonstrated. Despite the influence of proliferation-stimulating factors, cell clusters contained not only nestin-immunopositive stem cells, but also beta-tubulin-, vimentin-, and GFAP-positive cells differentiating by the neural pathway. Stem cells were localized on the surface of clusters. The percentage of stem cells in large clusters was lower than in small clusters.

Brain↗
PubMed2001

Histogenesis of hippocampus and neocortex isolated from postnatal rats in organotypic roller tube cultures of floating brain sections.

Floating sections of the hippocampus and neocortex isolated from 6-10-day-old rats retained their spatial cell organization after 2-week roller-tube culturing. Cell structure in CA1, Ca2, and CA3 fields, polymorphic layer of the fascia dentata and its medial and lateral limbs were revealed in sections of the dorsal hippocampus. In neocortical sections, cortical neurons and subcortical structure were preserved, however, some cortical fragments changed their configuration and formed spherical structures, where cortical neurons were located in the external layer without forming typical of neocortex 6-layer structure.

Animals↗
PubMed2001

[Ultrastructural plasticity in the hippocampus organotypic tissue culture].

Hippocampal cross sections of 7-9 day old rats were explanted onto semipermeable microporous membranes for 14-16 days followed by electron microscopic investigation. Besides the structures typical for adult hippocampus in vivo, substantial ultrastructural signs of metabolism and synaptic connections in explants were revealed: redistribution of polysomes and cisterns of granular endoplasmic reticulum, numerous pinocytotic invaginations, growth cones, somatic filopods, dotted (perforated) contacts, new formation of synapses and vacant postsynaptic sites. The data obtained indicate the active compensatory processes of plasticity, which ensure the maintenance of structure and function of hippocampal tissue in vitro.

Animals↗
PubMed2000

[The role of nitric oxide and other free radicals in ischemic brain pathology].

Nitric oxide (NO), an intercellular messenger and a normal metabolic product, takes an active part in the regulation of physiologically significant functions of the cardiovascular, immune, and nervous systems. At the same time when produced in excess amounts, NO as a free radical and an agent that gives rise to highly toxic oxidants (peroxynitrile, nitric dioxide, nitron ion), becomes a cause of neuronal damage and death in some brain lesions (parkinsonism, Alzheimer's disease, Huntington's chorea). Numerous experimental data show the ambiguous effects of NO on the development of cerebral infarct. NO as an active vasodilatory and antithrombogenic agent may reduce cerebral damage in early ischemia. There is evidence for the involvement of NO in the body's adaptation to oxygen starvation and ischemic tolerance formation. In the postischemic period, NO is a major factor of neuronal necrosis and apoptosis. The currently established ideas on the processes of cerebral NO production and on the pathogenetic mechanisms of this agent's cytotoxicity open up new vistas for selective blockers of various NO synthesis enzymes (neuronal, endothelial, glial cellular, and macrophagal and neutrophilic NO synthases) used in the treatment of acute vascular abnormalities of the central nervous system.

Animals↗
PubMed2000

[Effect of gangliosides on intensity of the lipid peroxidation process and structural changes in neuronal membranes, caused by toxic doses of glutamate].

We studied effects of gangliosides on the level of lipid peroxides and microviscosity of membrane lipid bilayer in primary dissociated cultures of cerebellar granule cells prepared from 8 day-old rats under conditions of neurotoxic effect of glutamate. It was found that glutamate (100 mkM) treatment of primary cultures activated the processes of lipid peroxidation and decreased microviscosity of neuronal membranes determined as a degree of pyrene excimerization. It was also shown that preincubation of granule cells with gangliosides did not prevent the accumulation of TBA-reactive products induced by glutamate. At the same time gangliosides significantly decreased the membrane-fluidizing effect caused by glutamate.

Animals↗
PubMed2000

Neuroprotective properties of nootropic dipeptide GVS-111 in in vitro oxygen-glucose deprivation, glutamate toxicity and oxidative stress.

Argon anoxia and glucose deprivation were used for modeling of ischemic damage in the cultures of cerebellar granule cells. Protective effect of peptide piracetam analogue GVS-111 was demonstrated. GVS-111 prevented neurodegeneration induced by glutamate and oxidative stress. In contrast to GVS-111, piracetam did not attenuate neurocytotoxic effect of glutamate.

2-Amino-5-phosphonovalerate↗
PubMed1998

[Mechanisms of neuronal calcium homeostasis destabilization caused by hyperstimulation of glutamate receptors].

The present paper summarizes the data obtained in studying the mechanisms of glutamate-induced deterioration of neuronal Ca2+ homeostasis. In the cultured mammalian central neurons, a short-term (< 1 min) glutamate (GLU, 100 mu) challenge is known to induce a readily reversible (transient) neuronal [Ca2+]i increase. In contrast, a long-term (15-30 min) GLU exposure leads to the appearance of high [Ca2+]i plateau or to the partial recovery of the increased [Ca2+]i. Experiments show that impaired [Ca2+]i recovery in the postglutamate period cannot be explained by the increased [Ca2+]i permeability of the neuronal membrane, as earlier considered. Moreover, a sustained elevation of [Ca2+]i during and after chronic GLU application is associated with a progressive decrease in Ca2+ permeability. The major cause of GLU-induced Ca2+ overload is the mitochondrial depolarization resulted from excessive Ca2+ influx into the mitochondria, the generation of free radicals and the opening of a "giant pore" in the inner mitochondrial membrane. This in turn suppresses both ATP synthesis and Ca2+ electrophoretic uptake into the mitochondrial matrix. In combination with [Ca2+]i-dependent acidification, this leads to the suppression of Ca2+ release from the cell via Na+/Ca2+ exchanger and Ca2+/H+ pump of the neuronal membrane. Therefore, [Ca2+]i recovery following a long-term GLU treatment becomes strongly or even irreversibly compromised.

Animals↗