Publications by authors named "Rakhmanova V"

Previously we found altered microglia-neuron interactions in the prefrontal cortex in schizophrenia. We hypothesized that microglia-neuron interactions may be dysregulated in the caudate nucleus in schizophrenia. A postmortem ultrastructural morphometric study was performed to investigate satellite microglia (SatMg) and adjacent neurons in the head of the caudate nucleus in 21 cases of schizophrenia and 20 healthy controls.

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Objective: To study the ultrastructure of microglia and neurons in contact with each other in the head of the caudate nucleus in continuous schizophrenia (CS) and paroxysmal-progressive schizophrenia (PPS) as compared to controls and to analyze correlations between the parameters of microglia and neurons in the control and schizophrenia groups.

Material And Methods: Post-mortem electron microscopic morphometric study of microglia and neurons in contact with each other was performed in the head of the caudate nucleus in 9 cases of CS, 10 cases of PPS and 20 controls without mental pathology. Group comparisons were made using analysis of covariance and Pearson correlation analysis.

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This study addressed the question of whether the interaction between neurons and satellite microglia (SatMg) is abnormal in schizophrenia. SatMg-neuron communication at direct contacts between neuronal soma is essential for neuroplasticity as SatMg can regulate neuronal activity. A postmortem ultrastructural morphometric study was performed to investigate SatMg and adjacent neurons in layer 5 of the prefrontal cortex in 21 cases of schizophrenia and 20 healthy controls.

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Objective: To study the ultrastructure of microglia adjacent to oligodendrocytes in white matter of the prefrontal cortex in continuous schizophrenia (CSch) as compared to controls and attack-like schizophrenia (ASch) and to perform correlation analysis between the parameters of microglia and adjacent oligodendrocytes previously detected in both clinical types of schizophrenia.

Material And Methods: Electron microscopic morphometric study of microglia adjacent to oligodendrocytes was performed in postmortem white matter of the prefrontal cortex (BA10) in 9 cases of CSch, 8 cases of ASch and 20 healthy controls. Group comparisons were made by ANCOVA and Pearson correlation analyses.

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Microglial activation has been proposed to contribute to the pathogenesis of schizophrenia. The present study addressed the questions of whether microglial reactivity is involved in the course of schizophrenia and is associated with aging. Transmission electron microscopy and morphometry were applied to estimate microglial density and ultrastructural parameters in layer 5 of the prefrontal cortex (BA10) in postmortem 21 chronic schizophrenia and 20 healthy control cases.

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Background: Some evidence support the notion that microglia activation in acute state of schizophrenia might contribute to damage of oligodendrocytes and myelinated fibers. Previously we found dystrophic changes of oligodendrocytes in prefrontal white matter in schizophrenia subjects displaying predominantly positive symptoms as compared to controls. The aim of the study was to verify whether microglial activation might contribute to dystrophic changes of oligodendrocytes in prefrontal gray matter in this clinical subgroup.

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Mast cells express high-affinity IgE receptor (FcεRI) on their surface, cross-linking of which leads to the immediate release of proinflammatory mediators such as histamine but also late-phase cytokine secretion, which are central to the pathogenesis of allergic diseases. Despite the growing evidences that mammalian target of rapamycin (mTOR) plays important roles in the immune system, it is still unclear how mTOR signaling regulates mast cell function. In this study, we investigated the effects of 3-benzyl-5-((2-nitrophenoxy) methyl)-dihydrofuran-2(3H)-one (3BDO) as an mTOR agonist on FcεRI-mediated allergic responses of mast cells.

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Microglial activation has been proposed to be involved in the pathophysiology of schizophrenia (SCZ). We hypothesized that dystrophic alterations of oligodendrocytes previously reported in the prefrontal white matter in SCZ might be associated with microglial activation in the acute state of SCZ. White matter of the prefrontal cortex (BA10) was studied in post-mortem brain tissue from 21 SCZ cases and 20 normal controls.

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Mast cells integrate innate and adaptive immunity and are implicated in pathophysiological conditions, including allergy, asthma, and anaphylaxis. Cross-linking of the high-affinity IgE receptor (FcεRI) initiates diverse signal transduction pathways and induces release of proinflammatory mediators by mast cells. In this study, we demonstrated that hyperactivation of mechanistic target of rapamycin (mTOR) signaling using the mTOR activator MHY1485 suppresses FcεRI-mediated mast cell degranulation and cytokine secretion.

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Aim: Previously the authors have reported the ultrastructural pathology and deficits of oligodendrocytes in gray and white matter of the prefrontal cortex in continuous paranoid schizophrenia. The aim of the present work was to study the effects of microglia on the ultrastructure of oligodendrocytes in white matter underlying the prefrontal cortex (BA10) in attack-like schizophrenia.

Material And Methods: Postmortem morphometric electron microscopic study of oligodendrocytes in close apposition to microglia was performed in white matter underlying the prefrontal cortex (BA10).

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Aim: Previously the authors have reported the ultrastructural pathology and deficit of oligodendrocytes in gray and white matter of the prefrontal cortex in schizophrenia. The aim of the study was to determine of the effects of microglia on the ultrastructure of oligodendrocytes in the white matter underlying the prefrontal cortex in continuous schizophrenia.

Material And Methods: Postmortem morphometric electron microscopic study of oligodendrocytes in close apposition to microglia was performed in white matter underlying the prefrontal cortex (BA10).

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Aim: Previously the authors have reported the ultrastructural pathology of myelinated fibers (MF) in the brain in schizophrenia. The aim of the present study was to compare the effect of disease course on ultrastructural changes of MF.

Material And Methods: Postmortem electron microscopic morphometric study of MF was performed in the prefrontal cortex, caudate nucleus and hippocampus in 19 cases of paranoid schizophrenia.

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Monocyte activation is consistently reported in patients with schizophrenia (SZ). We aimed to study the ultrastructure of monocytes and monocyte production of IL-1β in drug-free patients with SZ and controls. Monocytes from young (18-30 y.

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Monoamine oxidase activity was quantitatively assessed by cytochemical method in brain structures (layers III and V of the sensorimotor cortex, caudate nucleus, nucleus accumbens, hippocampal CA3 field) of rats of August line and Wistar population with high and low locomotor activity in the open fi eld test. Monoamine oxidase activity (substrate tryptamine) predominated in the nucleus accumbens of Wistar rats with high motor activity in comparison with rats with low locomotor activity. In August rats, enzyme activity (substrates tryptamine and serotonin) predominated in the hippocampus of animals with high motor activity.

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Objective: Neuroimaging studies showed abnormalities in frontal white matter (WM) in schizophrenia that were associated with clinical symptoms. Previously, we reported ultrastructural alterations of myelinated fibers and reduction in the numerical density of oligodendrocytes in BA 10 WM in patients with schizophrenia. We aimed to perform a qualitative and morphometric study of the ultrastructure of oligodendrocytes in BA 10 WM in schizophrenia and in normal controls.

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Objective: to study the effect of olanzapine on the ultrastructure of different populations of lymphocytes and lymphoblasts in patients with schizophrenia.

Material And Methods: Authors performed a morphometric study using electron microscopy of lymphocytes in 56 patients with schizophrenia treated for 8 weeks with olanzapine and 49 patients treated for 28 weeks with olanzapine before and after treatment. Authors estimated the frequency and ultrastructural parameters of small, large, large activated lymphocytes and lymphoblasts.

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Objective: To investigate the effect of olanzapine treatment on the ultrastructure of granulated platelets (GP) and vacuolated platelets (VP) and to find their association with platelet serotonin (PS) content and treatment efficacy in patients with schizophrenia.

Materials And Methods: Platelets of 49 patients with attack-like schizophrenia treated with olanzapine and 31 healthy people were explored. Electron microscopic morphometry of GP and VP was performed to estimate the ultrastructural parameters of platelets.

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Acetylcholinesterase activity was quantitatively evaluated by cytochemical method in brain structures (layers III and V of the sensorimotor cortex, caudate nucleus, nucleus accumbens, hippocampus CA3 field) of August and Wistar rats demonstrating high and low motor activity in the open field test. In August rats, acetylcholinesterase activity in the analyzed brain structures prevailed in animals with high motor activity in comparison with rats with low motor activity. In Wistar rats, the differences between the animals demonstrating high and low motor activity were less pronounced, but varied depending on the experimental series of studies.

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An aim of the study was to investigate the effect of olanzapine treatment on platelet ultrastructure and to search for its association with serotonin metabolism in patients with schizophrenia. Platelets of 59 patients with chronic (attack-like schizophrenia) treated with olanzapine and 31 health people were explored. Based on the data on the platelet ultrastructure, authors studied the content of functionally activated vacuolated platelets (VP) and less active granular platelets (GP) as well of platelet serotonin (PS).

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Objective: Previously the ultrastructural alterations of astrocytes have been reported in schizophrenia. Reduced dendritic arborization of the neurons in layer 5 of the prefrontal cortex has been found in schizophrenia. Authors hypothesized that the abnormalities in perineuronal astrocytes (PA) might contribute to these neuronal changes.

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Differences in the response of August rats' hippocampal field СА1 and СА3 neurons to the chronic haloperidol administration (a model of parkinsonism) were revealed by interferometric methods. Based on the morphochemical parameters (nuclear and cytoplasmic area, protein content and concentration), the changes of field СА1 neurons can be regarded as functionally active (all parameters are significantly higher than in controls), and those of field СА3 neurons - as initial stages of degeneration (the significant decrease of neuron sizes). The differences in the response found in this study can be associated with the functional characteristics of СА1 and СА3 fields.

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Objective: To evaluate the use of a commercially available 5-carboxyfluorescein-based, intramolecularly quenched, fluorescence resonance energy transfer (FRET) peptide substrate of renin for measurement of plasma renin concentration in cats.

Sample Population: Plasma samples obtained during a previous study of renal autograft ischemia-reperfusion injury in 10 cats and samples of fetal bovine serum containing recombinant human renin (rh-renin).

Procedures: Experiments involving samples of fetal bovine serum containing rh-renin were conducted to identify a suitable control vehicle, optimal substrate concentration, and appropriate duration of incubation.

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The hippocampus (CA3 field) was studied in rats with different behavioral characteristics. Protein contents in the neuronal cytoplasm and nuclei, as well as the size of neurons in animals predisposed to stress, poorly trained in a shuttle box, and exhibiting low locomotor activity in the open field were lower than in rats resistant to stress and characterized by high learning capacity and locomotor activity. Our results suggest that neuronal differences in the hippocampal CA3 field are associated with variations in learning capacity of animals.

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