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Background and Objectives: According to known experimental data, various metabolites of arachidonic acid have a vasoconstrictor or vasodilator effect, which in turn affects neuronal activity. The level of metabolite production can be influenced in several ways: by regulating oxygen levels or by glutamate-dependent increases in astrocytic calcium concentrations in response to neuronal activity. To analyze possible patterns of activity of nervous tissue in response to changes in the metabolic profile, a mathematical model was developed, within the framework of which computational experiments were carried out both in the local case and on spatial patterns. Materials and Methods: The work proposes a point model and its further extension for a spatially distributed system of connected neurogliovascular units. To test the performance of the model, we include an external influence leading to an increase in neuronal potassium and the occurrence of cortical depression, and an external influence on calcium activity, in order to analyze the influence of arachidonic acid metabolites on the process under study. Results: A new point model of the neurogliovascular unit has been developed that simulates the effect of arachidonic acid metabolites on cortical spreading depression, while expanding the point model to a spatially distributed case allowed us to determine the ways in which astrocytic activity influences the spatiotemporal characteristics of the wave of cortically spreading depression. Numerical studies of point and spatial models have confirmed the correspondence of the solutions to the observed experimental effects, including those associated with the peculiarities of the influence of arachidonic acid metabolites on the speed, area and lifetime of depression waves. It is assumed that in the future the results of the theoretical study can be used to find ways to return nervous tissue to the normal state from pathological conditions that occur with epilepsy, migraines and other neurodegenerative conditions associated with the occurrence of cortical depression waves.

Aim. To study pathomorphological signs of revascularization of perifocal areas of brain infarction in the dynamics of the acute period of the disease. Material and methods. Perifocal areas of brain infarction in patients who died at the 1st, 3rd, 7th, and 14th days were studied. General histopathological study was followed by 10 % ammonium silver impregnation and immunohistochemical examination using monoclonal antibodies Mo a-Hu CD34, Clone QBEnd/10 (“Thermo Fisher Scientific Inc.” – USA) and Mo a-Hu CD105 Endoglin were used. clone: SN6h1 (“DAKO”, Denmark). Vascular density and total cross-sectional area of vessels were studied. For the morphometric study, Videotest – Morphology 5.2.0.158 software (VideoTest LLC) was used. Statistical processing of the obtained data was carried out using the Statistica® for Windows 13.0 software. Results. According to the data of CD34 expression, from the 3rd day in the perifocal areas of brain infarction, the angiogenesis processes were increased: the density of blood vessels increased by 18.48 %, and the total cross-sectional area of vessels increased by 1.93 times. On the 7th day, the maximal vessel density and total cross-sectional area of vessels were registered in these areas; there was a vascular budding, formation of endothelial proliferates, and increased expression of CD105 on the vascular endothelium and pericytes, which indicates the active participation of the latter in angiogenesis. On the 14th day, blood vessel density and indicators of the total cross-sectional area of vessels decreased. During this period, the density of the astrocytes increased in the infarct’s perifocal areas with hypertrophy of their bodies and processes. Conclusions. According to CD34 and CD105 expression data, in the perifocal areas of cerebral infarction, the processes of angiogenesis gradually increase from the 3rd day manifesting by increase in the blood vessel density and total vascular cross-sectional area, as well as in the vascular budding and the formation of endothelial proliferates. Vascular remodeling is accompanied by increased density and hypertrophy of astroglia in the perifocal areas of cerebral infarction.

For many years, the topic of the development of suicidal behavior has remained relevant. Every year, there are more reports of new morphological changes in brain tissue, with particular emphasis on the effects of changes and the microenvironment on the functional activity of neurons and the relationship with the development of certain mental diseases. Because morphological changes are not always visible and apparent, immunohistochemical examination for glial fibrillary acid protein might be an additional diagnostic method. The presented literature review is an analytical evaluation of the current status of the topic of studying the morphology of macroglia, astrocytes, oligodendrocytes, and the bloodbrain barrier in suicide. According to generalized data, the most characteristic localizations of changes in the development of suicidal behavior are the suture nucleus and prefrontal and anterior cingulate cortex. There is evidence of a correlation between the development of suicidal behavior and an increase in inflammatory cytokines in the prefrontal cortex, a disruption in the connection between astrocytes and oligodendrocytes in the anterior cingulate cortex, and an indication of the involvement of the shell, striatum, preclinium, and wedge, orbitofrontal cortex in suicidal behavior formation. When examining the causes of death, determining the characteristic morphology of suicide death can potentially constitute an evidence base for confirming or excluding factors of suicide development. Further research is needed to form a clearer picture of the changes in relation to the practice of forensic medical examination; nonetheless, immunohistochemical analysis might be considered a potential method of evidence-based understanding suicide factors.

This paper addresses spatial aspects of reactive astrogliosis in the substantia nigra pars compacta (SNc) of the rat brain observed 40 and 70 days after the intracerebral 12 µg rotenone infusion. The infusion was shown to cause a marked increase in astrocyte density at both analyzed time points. Minimal spanning tree (MST) analysis was applied to analyze spatial patterns formed by nigral astrocytes. Spatial clusters of these cells, identified as disjoint MST subgraphs, were more numerous in the infused SNc tissue as compared with the control one. Size and density of clusters were significantly different between the infused and control areas 40 and 70 days after the infusion. In conclusion, the data suggests that rotenone-related astrogliosis in the substantia nigra includes changes in spatial patterns of astrocytes as well as transient spatial clustering of these cells. [ABSTRACT FROM AUTHOR]

Human memory functions on several levels. Primary is directly related to sensory imprinting and is localized in the thalamus. Human thinking is based on long-term memory and is formed in the areas immediately adjacent to the corresponding sensory analyzers in the cerebral cortex. Formal logic is a science investigating the basic axioms and principles of thinking; its conceptual apparatus reflects an idealization of multiple working structures and contacts existing in the cortex. In this theoretical research the author has comprehensively studied a qualitatively new conception of human thinking and memory based on the principles of psycholamarkism, neovitalism and systemevolutionary hierarchy. A special role in these processes is assigned to histone proteins and astrocytes. According to the author, astrocytes act as passive memory keepers, which carry an analog rather than digital code, closely interacting through biochemical connections between glio- and neurotransmitters. In addition, a separate line is also written about the still hard-to-explain abilities of some terrestrial unicums to hypercalculus and other miraculous mnemonic phenomena. The last section describes five fundamental principles and axioms of thought. [ABSTRACT FROM AUTHOR]

The article reflects the current position of the issue of morphologies of the pathways of intercellular circulation in the brain. There are covered main, known at present time, data on the features of the exchange between the spinal fluid and intercellular fluid, the ways of elimination of the intertissued fluid of the brain through the so-called “glymphatic system”, its components: transarterial, transvenous, and transglial ways of intercellular fluid outflow from brain tissue. It also raises the question of the role of glia namely astrocytes and ependymocytes – as the main cells forming the haemato-encephalic barrier and participating in the intercellular circulation.

Correlation between individual typological features like sex-related characteristics and low initial level of stress resistance and unfavorable prognosis of ischemic brain damage is shown. At the same time, the astrocytes’ participation in neuroplasticity in this disease represents the purpose of the study. The goal was to study the cerebral cortex astrocytes’ morphometric characteristics during the cerebral hypoxia in rats of different sexes with different stress tolerance levels. We performed the study with 72 Wistar rats. According to the Open Field test results all the animals were divided into two subgroups: with high and low level of stress tolerance. Both carotid arteries of the experimental group animals (48 animals) were bandaged. Animals were removed from the experiment at 21, 60 and 90 days after surgery. Glial fibrillary acidic protein (GFAP), a marker of mature astrocytes, was detected on histological sections of the central brain gyrus using primary polyclonal rabbit antibodies. Progressive decrease of the astrocytes’ numerical density and the number of first order processes were obtained during the study. It was less pronounced in animals with high stress tolerance and females. Increase of the processes’ distribution area was reliably detected. Area decreased after 90th day of the experiment. It is concluded that the astrocytes’ alteration develops earlier in animals with high stress tolerance and males, later in females (60 days) and animals with low stress tolerance (90 days).

Introduction. Astrocyte dysfunction is typical for many CNS pathologies, yet few experimental models of selective astrocyte damage, which would enable a fuller understanding of the role of astrocytes in the pathogenesis of neurodegenerative disorders, exist. Study aim to characterize the morphological brain changes with the administration of -aminoadipic acid (L-AA), a glial toxin, into the rat striatum and to assess the effect of astrocyte dysfunction on motor activity in animals. Materials and methods. Astrocyte damage was achieved by administering L-AA (100 g in 5 l) into the rats right striatum; the same volume of phosphate-buffered saline was injected into the left hemisphere as a control. On the third day after L-AA administration, motor impairment was assessed with normal and reduced dopaminergic neurotransmission; the latter was achieved with administration of the -methyl-p-tyrosine, a tyrosine hydroxylase inhibitor. The immunohistochemical studies included assays for glial fibrillary acidic protein (GFAP), neuronal nuclear antigen (NeuN), and tyrosine hydroxylase. Results. When dopamine synthesis was inhibited, damage to the striatal astrocytes, which was confirmed by immunohistochemistry, caused a reduction in motor activity in the open field test and an increase in the number of errors in the beam walking test. When dopaminergic transmission was reduced through the inhibition of tyrosine hydroxylase by -methyl-p-tyrosine, the motor disturbances caused by astrocyte damage sustained and worsened. Conclusion. The obtained data indicate the regulatory role of astroglia in the nigrostriatal system and emphasize the possible contribution of glial dysfunction to the motor disturbances in Parkinsons disease.

Цель: выделение клеток волокнистой астроцитарной глии на гистологических срезах гиппокампов при использовании двух различных растворов солей серебра. Материал и методы. Гистологические срезы гиппокампов кроликов, разделенные на две группы, импрегнировали растворами азотнокислого и бромистого серебра. Результаты. На гистологических срезах гиппокампов 1-й группы импрегнировались коротколучистые волокнистые астроциты (ВА). Около круглых ядер наблюдали различную плотность расположения глиофибрилл. Во 2-й группе импрегнировались длиннолучистые ВА с радиально расходящимися тонкими глиофибриллярными отростками. Заключение. Правильное представление об истинной структуре многоотростчатых клеток (содержащих глиофибриллы) можно получить при сравнительном изучении и анализе гистологических препаратов, окрашенных с помощью различных методов импрегнации солями серебра.

Among various cellular populations, ERMs contain cells with contractile features typical of myofibroblasts. This type of cells provides collagen producing and facilitates membrane contraction. The identification of ERM morphological elements at different stages of its formation remains a topical question.Purpose. To investigate the cells morphological features in a qualitative composition of epiretinal membranes in patients with different visual acuity.Material and methods. All patients were divided into 3 equal groups of 20 patients (20 eyes), depending on the initial best corrected visual acuity (BCVA). Samples of ERM were obtained from 60 patients during microsurgical operations with subseuqent. There was performed an immunohistochemistry to recognize: glial acidic fibrillary protein (GFAP), TGF-β1, α-SMA actin, cellular retinaldehyde-binding protein (CRALBP), fibronectin, CD68, CD45, aswell as collagen of II, IV, VI types.Results. Specimens, removed from eyes with a higher visual acuity, showed a more cell viability than specimens, removed from eyes with a lower visual acuity. Comparing these specimens we found significant differences in cell viability depended on cell proliferation and transdifferentiation. Our results revealed that ERMs are characterized by the intensive decreasing of glial acidic fibrillary protein (GFAP) expression and competitive increasing α-SMA actin myofibroblast-like cells in time. As a result, we detected a diffuse presence of α-SM actin–positive myofibroblasts containing TGF-β1 and collagen expression at late stages. Conclusion. Immunocytochemical analysis helps to identify the pathomorphological changes of ERM samples and to determine mechanisms of ERM formation in patients with a different severity of pathological process.

Introduction. The perifocal zone of cerebral infarction contains dying and reactively altered neurons whose fate depends on the type of intracellular interactions and, in particular, on the response of astrocytes partaking both in neuronal damage and neuroprotection. The features of the response of astrocytes to ischemic injury and the role of their activation in gliosis have been studied insufficiently. Objective. To evaluate the changes in astroglia in the perifocal zone of cerebral infarction depending on its reproduction time by immunomorphology and computerassisted morphometry. Materials and methods. Infarction was induced in the left hemisphere of rat brain cortex (n=10) by middle cerebral artery occlusion. Astrocyte distribution and shape were assessed on day 3 and 21 after surgery; localization of gliofibrillar acidic protein (GFAP), aquaporin 4 (AQP4), and glutamine synthetase (GlnS) in the perifocal zone was measured. Results. Astrocyte shape and distribution, as well as GFAP expression, significantly altered depending on time that has passed since the infarction and distance to the injury focus. On day 3, the area occupied by astrocyte processes decreased by 15% of the control value, while increasing by 35% on day 21. Expression of GlnS and AQP4 near the infarction focus decreased on day 3, while opposite changes were observed on day 21. Redistribution of the studied proteins in processes of reactive astrocytes was also detected. Two morphological types of astrocytes were differentiated: the scarring polarized astrocytes, which were characterized by redistribution of marker proteins in processes, and the moderately altered transiently activated ones. Conclusions. Astrocytes were found to be heterogeneous in the perifocal zone of cerebral infarction; a dependence between changes in their structure and function and the distance to the injury focus and time that passed after the infarction was revealed. The scarring and transiently activated astrocytes, which play different roles in remodeling and repair of ischemic neural tissue in the perifocal zone of cerebral infarction, were characterized by immunohistochemical and morphometric analysis.

Current experimental models of the blood-brain barrier (BBB)in vitro used for studying mechanisms of permeability and intercellularcommunication are discussed in this review. At present,monolayer, multilayer and computer models are in use for theabove-mentioned purposes. Primary isolated cells that make upthe models in vitro may have brain and non-brain origin. Inaddition, transplantable cell lines and co-cultured cells could beused for modeling BBB in vitro.

Purpose: to obtain morphological data to identify microglia on histological sections of hippocampus of rabbits using silver salt impregnation. Material and methods. Histological sections of hippocampus of rabbits impregnated with salt deposited silver. Using the Rio Hortega method for detecting fibrous glia, choose the desired chemical composition and acid-base parameters of the silver solution and reducing agent for the detection of microglia. Results. In histological sections of the hippocampus revealed microglia contrast with branched spikes and cells without shoots with thin flagellums. Conclusion. In visiting the experiments carried out in natural conditions, it is crucial to conduct biomedical research in the shortest possible time. We need to get not only the functional results of research, but also by their morphological, substantiating the data. The present method of impregnation microglia can be used as a rapid method for the morphological study of cerebral blood flow and neural tissue hypoxia.

Abstract: A number of pathophysiologic manifestations can be distinguished that are characteristic of both epilepsy and other common vascular, demyelinating and degenerative central neural system (CNS) diseases. This is a consequence of neural system's endogenizing capacity that determines the possibility of its response with non-specific typical pathologic processes to various pathologies and at different levels of structural and functional organization. The current concept of the blood-brain barrier (BBB) structural and functional organization fundamentally differs from those previously suggested: by early 1980s it became recognized that the BBB represents a dynamic morphofunctional entity, formed by brain capillary endothelial cells and periendothelial structures. This reflects the accumulation of knowledge on this subject that received close attention of scientific and academic communities resulting in an increased number of fundamental and applied BBB studies. In order to realize the role of the BBB in CNS functioning in normal and pathologic settings, it is necessary to clearly understand its development during the ontogeny, as well as exogenous and endogenous factors that can lead to BBB damage ('disrupture'). This will help to verify the number of markers that allow adequate evaluation of the BBB and neural tissue condition, and also to chose a strategy for the management of patients with CNS disorders.

Aim: identification of astrocytic glia cells impregnated to determine the hypoxic changes in nerve tissue. Material and methods. Condition of hypoxia was simulated in laboratory rats with "jar hypoxia". For the impregnation of histo-logical sections were used as a basis for the method of Rio-Gortega. Results. Silver impregnation method revealed several morphological forms of astrocytic cells in hypoxic changes in the nervous tissue of the brain. Conclusion. There were marked morphological brain astrocyte cell forms reflecting their functional state. Traced compensatory changes astrocytic cell depletion of these processes and the appearance of pathological morphological characters, up to the fragmentation and destruction of cells.

We reviewed the role of oxidative stress (OS) in the pathogenesis of ischemic (IS) and hemorrhagic stroke (HS). OS plays a major role in programmed cell death, increased permeability of the blood-brain barrier, astroglial and microglial activation, and local inflammatory response. We also reviewed the current state of neuro- and cytoprotection studies and their translation in clinical practice. With respect to experimental and clinical data the efficacy of long term administration of multimodal cytoprotective drug with antioxidant effect - ethylmethylhydroxypyridine succinate (Mexidol) is discussed during the acute and early recovery period after stroke.

In the central nervous system of mammals, there are specialized areas in which neurogenesis - neurogenic niches - is observed in the postnatal period. It is believed that astrocytes in the composition of neurogenic niches play a significant role in the regulation of neurogenesis, and therefore they are considered as a promising "target" for the possible control of neurogenesis, including the use of optogenetics. In the framework of this work, we formed an in vitro model of a neurogenic niche, consisting of cerebral endothelial cells, astrocytes and neurospheres. Astrocytes in the neurogenic niche model expressed canalorodopsin ChR2 and underwent photoactivation. The effect of photoactivated astrocytes on the expression profile of neurogenic niche cells was evaluated using immunocytochemical analysis methods. It was found that intact astrocytes in the composition of the neurogenic niche contribute to neuronal differentiation of stem cells, as well as the activation of astroglia expressing photosensitive proteins, changes the expression of molecules characterized by intercellular interactions of pools of resting and proliferating cells in the composition of the neurogenic niche with the participation of NAD+ (Cx43, CD38, CD157), lactate (MCT1). In particular, the registered changes reflect a violation of the paracrine intercellular interactions of two subpopulations of cells, one of which acts as a source of NAD+, and the second as a consumer of NAD+ to ensure the processes of intracellular signal transduction; a change in the mechanisms of lactate transport due to aberrant expression of the lactate transporter MCT1 in cells forming a pool of cells developing along the neuronal path of differentiation. In general, with photostimulation of niche astrocytes, the total proliferative activity increases mainly due to neural progenitor cells, but not neural stem cells. Thus, optogenetic activation of astrocytes can become a promising tool for controlling the activity of neurogenesis processes and the formation of a local proneurogenic microenvironment in an in vitro model of a neurogenic niche.

The review highlights the current understanding of the role of autoimmune neuroinflammation in the pathogenesis of vascular, neurodegenerative and other diseases of the nervous system. The mechanisms of the response of the resident cells of the central nervous system (microglia, astrocytes) and peripheral cells of the immune system are considered. Possible therapeutic potential of phosphodiesterase inhibitors, which have antiplatelet properties and the ability to suppress autoimmune inflammation, are outlined. The authors consider dipyridamole, an inhibitor of phosphodiesterase, as a promising drug.

Neurogenesis is a complex process which governs embryonic brain development and is importants for brain plasticity throughout the whole life. Postnatal neurogenesis occurs in neurogenic niches that regulate the processes of proliferation and differentiation of stem and progenitor cells under the action of stimuli that trigger the mechanisms of neuroplasticity. Cells of glial and endothelial origin are the key regulators of neurogenesis. It is known that physiological neurogeneses is crucial for memory formation, whereas reparative neurogenesis provides partial repair of altered brain structure and compensation of neurological deficits caused by brain injury. Dysregulation of neurogenesis is a characteristics of various neurodevelopmental and neurodegenerative diseases, particularly, Alzheimer's disease which is very important medical and social problem. In the in vitro model of the neurogenic niche using hippocampal neurospheres as a source of stem/progenitor cells and astrocytes, we studied effects of astrocyte activation on the expression of markers of different stages of cell proliferation and differentiation. We found that aberrant mechanisms of development of stem and progenitor cells, caused by the beta-amyloid (Aβ1-42), can be partially restored by targeted activation of GFAP-expressing cells in the neurogenic niche.

Age-related neurodegenerative diseases, including Parkinson's disease, are characterized by a number of pathomorphological signs, such as neuron loss in certain brain structures, gliosis, iron accumulation. However, the literature indicates that these signs can also be observed during normal (physiological) aging. The aim of our work was to evaluate qualitative and quantitative morphochemical changes in neurons and neuroglia, and also to localize iron (II) compounds in the human striatum during physiological aging. In the old age group, compared with the mature one, the size of the neuron bodies was significantly smaller, the neuronal distribution density did not differ, but the distribution density of both the overall glia and astrocytes was significantly higher. In the old age group, the accumulation of iron (II) compounds were seen along the walls of the vessels, as well as inside the cytoplasm of neurons and glial cells. We conclude that the results obtained may serve as a basis for the comparative study of the neurodegenerative process and for the earlier and more accurate diagnosis of neurodegenerative diseases associated with aging, including Parkinson's disease.

Aim: To study the changes in the morphological and morphometric parameters of immunopositive astrocytes of the amygdala in absence epilepsy depending on hormonal profile., Material and Methods: Adult female WAG/Rij rats were used as experimental subjects. The astrocytes were detected on serial sections using a reaction to glial fibrillary acidic protein (GFAP) with pre-stained hematoxylin. Quantitative analysis was carried out for a 204.8´153.6 μm 2 field of view., Results: In the control group, astrocytes had a relatively regular stellate form and GFAP was moderately expressed in their bodies and processes. The number of astrocytes was 18.20±2.87, and their area was 164±3.29 μm 2 . After ovariectomy, a high expression of the protein, both in the bodies and in the processes of astrocytes, increasing the cell size to 188.85±4.97 μm 2 (p<0.05) was observed. The astrocytes increased to 34.55±3.03 (p<0.05). In addition, the deformation of the processes and their diffuse defibration were observed. After hormone replacement therapy, a decrease in GFAP expression was detected, the area of astrocytes became smaller in comparison with the group after ovariectomy: 173.54±5.48 μm 2 (p<0.05). Morphological changes in glial cells were manifested as a decrease in the size of their bodies, the processes became smooth without diffuse sprouting and swelling, which is probably associated with neuroprotective functions of estradiol., Conclusion: Thus, the results of our study demonstrated that the deficiency of female sex hormones led to the increase in both the amount and area of astrocytes in the anterior cortical nucleus of the amygdala, and hormone replacement therapy positively affected the structural and quantitative characteristics of astrocytes due to the endogenous protective role of estradiol.

The objective of the present study was the development of the additional forensic medical criteria for the diagnostics of the intravitality and prescription of the burning injury making use of the morphological changes in the cerebellar cortex. A total of 82 cases of the death from the second- and third a, b-degree flame burns in 63 men and 19 women at the age from 20 to 65 years were available for the analysis. The condition of the cerebellar cortex was evaluated within 0 to 72 hours after the trauma had been inflicted. The routine histological staining technique using hematoxylin and eosin were employed as well as the Nisslin staining carried out in the combination with the immunohistochemical reaction based on the application of the antibodies against the glial fibrillary acidic protein (GFAP). In the case of death during the acute period after the burning injury, the histological study revealed a characteristic complex of the morphological features including the acute swelling of neurons, the increasing expansion of perivascular and pericellular spaces, as swell as hyperoxyphilia of microglia. The astrocytes of cortical II-III layers proved highly sensitive to tissue hypoxia as appears from their reaction with anti-GFAP antibodies. It is concluded that the results of the evaluation of the blood supply of the cerebral hemisphere cortex with the use of immunohistochemical methods may be helpful as the additional criteria for the purpose of forensic medical documentation of intravitality and prescription of the burning injury.

Aim: To investigate the expression of transporters of different neurotransmitters (glutamate, aspartate, lactate, choline) in the culture of astrocytes isolated from different regions of the brain (cortex, hippocampus and brainstem) in 3- and 11-day rats., Material and Methods: An experimental study was performed on 24 3- (n=12) and 11-days (n=12) old rats (Rattus norvegicus). The results of high-performance sequencing were analyzed., Results: The expression of glutamate and aspartate transporters in the brainstem of 3-day rats was higher than in other regions, however, an opposite effect was observed in 11-day rats. The expression of lactate transporters with age became identical to those of the cortex., Conclusion: The data demonstrate the particular qualities of neuro-astrocytic connections and the important role of astrocytes in signal transmission. Results of the study performed by using genetic methods developed by the authors for the study of neurotransmitter transporters make it possible to recommend these methods to control the neurogenesis and neurohomeostasis, including in cerebrovascular and neurodegenerative diseases.

Aim: To analyze the histological features of changes in the brain tissue after ischemic stroke., Material and Methods: Brain tissue samples obtained in autopsy from 9 people died as a result of a left middle cerebral artery ischemic stroke from 3 to 7 days after admission were studied. Tissue samples were taken from 3 areas of the brain: 1) contiguous to the tissue necrotic damage site zone, 2) 5-10 cm distant from the previous one, 3) the contralateral hemisphere zone symmetrical to damage site. Samples were Nissl and hematoxylin-eosin stained. Detection of p53 protein, NSE, GFAP was performed by indirect immunoperoxidase immunohistochemistry., Results: A decrease in the total number of neurons and glial elements, their spatial redistribution, change in cell structure and their functional activity was found. The changes of the artery wall and impaired regional blood flow were detected. The more intense NSE reactivity; p53-positive neurons, reduced neuron-astrocytes distance were identified in zones 2 and 3., Conclusion: Ischemic stroke is accompanied by severe histological changes. These changes with varying degrees of severity occur both in the areas adjacent to necrotic core, and in remote areas, and it is a substrate for neuroplasticity.

Hepatic encephalopathy is a common neuropsychiatric complication of serious liver diseases and serves as a marker for worsening of their course and increasing the risk of death. The principal pathogenesis factors of hepatic encephalopathy is the excessive formation of ammonia and its accumulation by astrocytes. A key role in the prevention and treatment of hepatic encephalopathy is played by drugs that prevent hyperammonemia and promote the removal of ammonia from the body, namely lactulose, rifaximin and L-ornithine-L-aspartate. L-ornithine-L-aspartate has proven clinical effectiveness in the treatment of hepatic encephalopathy, prevents the transformation of minimal hepatic encephalopathy into overt forms, increases the tolerability of psychotropic drugs used in the treatment of alcohol dependence, and improves cognitive functions.

β-adrenergic neurotransmission is an important factor regulating brain activity such as neuronal and glial survival, plasticity, membrane transport or cellular metabolism. Intracellular β-adrenergic signaling, via a stimulatory G protein (Gs), activates two major down-stream effectors, i.e., adenylyl cyclase (AC) and cAMP-dependent protein kinase A (PKA). The aim of this work was to study the ability of endogenous (adrenaline and noradrenaline) and exogenous (isoprenaline) β-adrenergic receptor agonists to increase cAMP in different types of nerve cells. Moreover, we wanted to precisely identify the receptor isoform involved in the observed phenomenon using selective β1-, β2- β3-adrenoceptor blockers. In an additional study, the negative influence of hypoxia on the AC/cAMP intracellular signaling system was tested. The study was conducted in parallel on rat primary glial (astrocytes) cultures, primary neuronal cultures, C6 glioma cells and human T98G glioma cells. The formation of [^(3)H] cAMP by agonists and antagonists was measured in [^(3)H] adenine prelabeled cells under normoxic and hypoxic conditions. The obtained results revealed that adrenaline, noradrenaline and isoprenaline strongly stimulated cAMP production in all tested cell types (with highest potency in C6 glioma cells). In glial and neuronal cells the adrenaline-evoked cAMP effect was mediated mainly by the β1-adrenoceptor, whereas in tumor cells the effect was probably mediated by all three β-subtype specific drugs. The AC/cAMP intracellular signaling system is affected by hypoxic conditions. Considering both physiological and therapeutic importance of β-family receptors the present work characterized the β-adrenoceptor-mediated cAMP signal transduction pathway in different nerve cells in normoxic and hypoxic conditions. The proposed in vitro model of hypoxic conditions may serve as a good model system to study the biological effects of endogenous catecholamines as well as potential therapeutics targeting adrenergic receptors, which are impaired during ischemia in vivo.

The authors studied the traits of psychotic attacks in 40 patients with terminal stages of chronic renal insufficiency. They were expressed in atypical delirious, delirio-amentive and amentive conditions. 8 cases were studied morphologically. The pathological process in the brain was characterized as toxico-dyshomeostatic encephalopathy. The pathogenesis of such disorders is discussed.

The reaction of the cerebral cortex glia to alcohol was studied in rats subjected to alcoholic intoxication. Use was made of the Nissl and Golgi method. In 20 days of alcohol intoxication (a 35% solution) the amount of the perineuronal and total glia, as calculated in stratum V of the sensomotor cortex, was found to increase, this increase being statistically significant. This was accompanied by changes of the glia cell metabolism (as was indicated by intensification of the glia impregnation properties) and by formation of compensatory glia-dendrite "contacts", probably, for maintaining the vital activity of the alcohol-affected neurons. Later (in 2, 4, 8, 12, and 15 months), along with the decrease of the number of neurons and the proliferation of the glia, there appeared signs of the latter's dystrophic changes. This is undoubtedly reflected on the cerebral cortex function.

Histological methods demonstrated that the use of psychopharmacological drugs in schizophrenic patients does not remove the characteristic neuron pathology (shrinkage, atrophy, lipofuscin dystrophy, cytolysis), but increases the metabolic processes in the intact nervous cells (an increase in the volume and basophilia in the cytoplasma, an enlargement of nuclei and nucleoli) and the glia activity (an increase in the amount of perineuronal satellites, general glia and the glioneuronal index). It is believed that the treatment does not remove the organic brain defect, but stimulates the metabolic processes in the CNS.

By means of computer analysis, size distribution of neurons and glial cells together with the label of 3H-thymidin labelled cells were studied in cytoarchitectonic layers of the field 1 in the mouse parietal cortex injected with the isotope on the 5th day of life and killed 1 month later. In some animals, 3 days before 3H-thymidin injection, the parietal region in the right hemisphere was perforated. The labelled cells were subdivided into 2 groups according to their size: astrocytes (A) and small gliocytes (mg). Labelled A and mg were stated to be rather evenly distributed along the cytoarchitectonic layers in the field 1. The trauma performed resulted in increasing amount of the labelled A and MG in the operated hemisphere. Uniformity in distribution of the labelled A and mg, occupying the position of satellites, did not change considerably at the trauma, in spite of general quantitative increase of the labelled glial cells. One month after the trauma, body dimentions of the mice labelled with A and mg did not considerably differ from those of intact animals, while the size of nerve cells increased. Thus, neurons in the parietal cortex of a growing brain respond to brain trauma with hypertrophy of cell bodies, and glial populations--with increase of their number.

The use of monolayer brain cell cultures from humans who had died of amyotrophic leukospongiosis and from animals with experimentally induced diseases allowed the authors to explore pathogenetic contribution of astrocytes to this disease. Morphofunctional heterogeneity of astrocyte population as well as the pathologic involvement of some of the cells were demonstrated, using light and electron microscopy and cytochemical technics.