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Dendritic spine density changes and homeostatic synaptic scaling: a meta-analysis of animal studies
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01.01.2022 |
Moulin T.C.
Rayêe D.
Schiöth H.B.
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Neural Regeneration Research |
10.4103/1673-5374.314283 |
0 |
Ссылка
Mechanisms of homeostatic plasticity promote compensatory changes of cellular excitability in response to chronic changes in the network activity. This type of plasticity is essential for the maintenance of brain circuits and is involved in the regulation of neural regeneration and the progress of neurodegenerative disorders. One of the most studied homeostatic processes is synaptic scaling, where global synaptic adjustments take place to restore the neuronal firing rate to a physiological range by the modulation of synaptic receptors, neurotransmitters, and morphology. However, despite the comprehensive literature on the electrophysiological properties of homeostatic scaling, less is known about the structural adjustments that occur in the synapses and dendritic tree. In this study, we performed a meta-analysis of articles investigating the effects of chronic network excitation (synaptic downscaling) or inhibition (synaptic upscaling) on the dendritic spine density of neurons. Our results indicate that spine density is consistently reduced after protocols that induce synaptic scaling, independent of the intervention type. Then, we discuss the implication of our findings to the current knowledge on the morphological changes induced by homeostatic plasticity.
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Thiamine and benfotiamine counteract ultrasound-induced aggression, normalize AMPA receptor expression and plasticity markers, and reduce oxidative stress in mice
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15.09.2019 |
Gorlova A.
Pavlov D.
Anthony D.
Ponomarev E.
Sambon M.
Proshin A.
Shafarevich I.
Babaevskaya D.
Lesсh K.
Bettendorff L.
Strekalova T.
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Neuropharmacology |
10.1016/j.neuropharm.2019.02.025 |
1 |
Ссылка
© 2019 Elsevier Ltd The negative societal impacts associated with the increasing prevalence of violence and aggression is increasing, and, with this rise, is the need to understand the molecular and cellular changes that underpin ultrasound-induced aggressive behavior. In mice, stress-induced aggression is known to alter AMPA receptor subunit expression, plasticity markers, and oxidative stress within the brain. Here, we induced aggression in BALB/c mice using chronic ultrasound exposure and examined the impact of the psychoactive anti-oxidant compounds thiamine (vitamin B1), and its derivative benfotiamine, on AMPA receptor subunit expression, established plasticity markers, and oxidative stress. The administration of thiamine or benfotiamine (200 mg/kg/day) in drinking water decreased aggressive behavior following 3-weeks of ultrasound exposure and benfotiamine, reduced floating behavior in the swim test. The vehicle-treated ultrasound-exposed mice exhibited increases in protein carbonyl and total glutathione, altered AMPA receptor subunits expression, and decreased expression of plasticity markers. These ultrasound-induced effects were ameliorated by thiamine and benfotiamine treatment; in particular both antioxidants were able to reverse ultrasound-induced changes in GluA1 and GluA2 subunit expression, and, within the prefrontal cortex, significantly reversed the changes in protein carbonyl and polysialylated form of neural cell adhesion molecule (PSA-NCAM) expression levels. Benfotiamine was usually more efficacious than thiamine. Thus, the thiamine compounds were able to counteract ultrasound-induced aggression, which was accompanied by the normalization of markers that have been showed to be associated with ultrasound-induced aggression. These commonly used, orally-active compounds may have considerable potential for use in the control of aggression within the community. This article is part of the Special Issue entitled ‘Current status of the neurobiology of aggression and impulsivity’.
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How regularities of mortality statistics explain why we age despite having potentially ageless somatic stem cells
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01.02.2018 |
Khalyavkin A.
Krut’ko V.
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Biogerontology |
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0 |
Ссылка
© 2017, Springer Science+Business Media B.V. Researchers working in the area of ageing have found numerous manifestations of this process at the molecular biological level, including DNA and protein damage, accumulation of metabolic by-products, lipids peroxidation, macromolecular cross-linking, non-enzymatic glycosylation, anti-oxidant/pro-oxidant misbalance, rising of pro-inflammatory cytokines, etc. This results in an increase in the proportion of cells in growth arrest, reduction of the rate of information processing, metabolic rate decrease, and decrease in rates of other processes characterizing dynamic aspects of the organism’s interaction with its environment. Such staggering multilevel diversity in manifestation of senescence precludes (without methodology of systems biology) development of a correct understanding of its primary causes and does not allow for developing approaches capable of postponing ageing or reducing organisms’ ageing rate to attain health preservation. Moreover, it turns out that damage production and damage elimination processes, the misbalance of which results in the ageing process, can to a large extent be regulated by external signals. The purpose of this report is to provide evidence supporting this view and its compatibility with the regularities of mortality statistics, because the main idea is very simple. Even potentially a non-senescent but certainly not immortal body must start to age under inadequate conditions (like a non-melting piece of ice taken out from the deepfreeze inevitably start to melt at the temperatures above zero Celsius). This conclusion is totally consistent with existing patterns of mortality and with agelessness potential of somatic stem cells. Therefore, there is no need to build up and explore too complicated, computational and sophisticated systems models of intrinsic ageing to understand the origin of this mainly extrinsic root cause of natural ageing, which is controlled by environmental signals. In our case, a simple phenomenological black-box approach with Input–Output analysis is ample. Here Input refers to the environmentally dependent initial force of mortality, whereas Output is a rate of age-related increase of mortality force.
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Correction of anxiety disorders: Focus on a comorbid patient
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01.01.2018 |
Shavlovskaya O.
Kuznetsov S.
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Terapevticheskii Arkhiv |
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0 |
Ссылка
© 2018 Media Sphera Publishing Group. All rights reserved. The exact cause of the development of anxiety disorders (AD) in present time has not been fully established and is a subject of debate in many countries. Interest in studying the mechanisms of action of proteins of S100 group, in particular, neurospecific protein S100b, is caused by its participation in processes of integrative activity of brain/neuron and development of diseases of nervous system. The functions of S100 proteins determine their influence on synaptic plasticity and participation in the regulation of stress-realizing and stress-limiting systems, the imbalance of which (primarily, the insufficiency of the GABA-ergic system) is the neurobiological basis of the majority of anxiety-depressive pathologies. Preparations regulating the activity of S100 protein have a distinct clinical anti-anxiety effect and additionally contribute to the restoration of neuronal plasticity processes.
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The influence of succinate-containing drugs on the process of neuroplasticity after ischemic stroke
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01.01.2018 |
Ekusheva E.
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Eksperimental'naya i Klinicheskaya Farmakologiya |
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0 |
Ссылка
© 2018 Izdatel'stvo Meditsina. All rights reserved. Succinate is an endogenous substrate of the human organism that participates in various redox processes, reactions of the Krebs cycle, and the mitochondrial oxidation chain. This universal intracellular metabolite plays an important role in the regulation of physiological, metabolic, and energy-producing processes. The article discusses the issues of neuroplasticity, the importance of correction of energy deficiency, oxidative stress and other pathophysiological processes, and maintenance of adequate functional activity of neuronal structures after cerebral circulation disorders. The problems of neuroprotective therapy in ischemic stroke, which is pathogenetically justified in all stages of restorative treatment after cerebrovascular accident, are considered. Cytoflavin is one of the most studied original cytoprotectors, which demonstrated safety, efficacy, and good tolerability. Results of numerous clinical trials revealed significant positive clinical and morphological dynamics of cytoflavin administration in patients after ischemic stroke.
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Apoptosis as a systemic adaptive mechanism in ischemic stroke
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01.01.2018 |
Sergeeva S.
Savin A.
Litvitsky P.
Lyundup A.
Kiseleva E.
Gorbacheva L.
Breslavich I.
Kucenko K.
Balyasin M.
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Zhurnal nevrologii i psikhiatrii imeni S.S. Korsakova |
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0 |
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This paper presents a literature review considering the role and mechanism of apoptosis in the pathogenesis of ischemic stroke (IS). The authors introduce a new concept: the functional request of the patient as a set of external (the nature and intensity of rehabilitation measures, characteristics of everyday life, diet, etc.) and internal (genetic factors, internal picture of the disease, availability of rental and other psychological facilities and etc.) attributes. This concept allows a new angle in understanding the pathogenesis of IS and creates fundamental and clinical potential for more successful approaches to therapy and rehabilitation after IS.
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Corrigendum: Early Growth Response Gene-2 Is Essential for M1 and M2 Macrophage Activation and Plasticity by Modulation of the Transcription Factor CEBPβ
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01.01.2018 |
Veremeyko T.
Yung A.
Anthony D.
Strekalova T.
Ponomarev E.
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Frontiers in immunology |
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0 |
Ссылка
[This corrects the article DOI: 10.3389/fimmu.2018.02515.].
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Pro-neurogenic, memory-enhancing and anti-stress effects of DF302, a novel fluorine gamma-carboline derivative with multi-target mechanism of action
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01.01.2018 |
Strekalova T.
Bahzenova N.
Trofimov A.
Schmitt-Böhrer A.
Markova N.
Grigoriev V.
Zamoyski V.
Serkova T.
Redkozubova O.
Vinogradova D.
Umriukhin A.
Fisenko V.
Lillesaar C.
Shevtsova E.
Sokolov V.
Aksinenko A.
Lesch K.
Bachurin S.
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Molecular Neurobiology |
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9 |
Ссылка
© Springer Science+Business Media New York 2016. A comparative study performed in mice investigating the action of DF302, a novel fluoride-containing gamma-carboline derivative, in comparison to the structurally similar neuroprotective drug dimebon. Drug effects on learning and memory, emotionality, hippocampal neurogenesis and mitochondrial functions, as well as AMPA-mediated currents and the 5-HT6 receptor are reported. In the step-down avoidance and fear-conditioning paradigms, bolus administration of drugs at doses of 10 or 40 mg/kg showed that only the higher dose of DF302 improved long-term memory while dimebon was ineffective at either dosage. Short-term memory and fear extinction remained unaltered across treatment groups. During the 5-day predation stress paradigm, oral drug treatment over a period of 2 weeks at the higher dosage regimen decreased anxiety-like behaviour. Both compounds supressed inter-male aggression in CD1 mice, the most eminent being the effects of DF302 in its highest dose. DF302 at the higher dose decreased floating behaviour in a 2-day swim test and after 21-day ultrasound stress. The density of Ki67-positive cells, a marker of adult neurogenesis, was reduced in the dentate gyrus of stressed dimebon-treated and non-treated mice, but not in DF302-treated mice. Non-stressed mice that received DF302 had a higher density of Ki67-positive cells than controls unlike dimebon-treated mice. Similar to dimebon, DF302 effectively potentiated AMPA receptor-mediated currents, bound to the 5-HT6 receptor, inhibited mitochondrial permeability transition and displayed cytoprotective properties in cellular models of neurodegeneration. Thus, DF302 exerts multi-target effects on the key mechanisms of neurodegenerative pathologies and can be considered as an optimized novel analogue of the neuroprotective agent dimebon.
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ROLE OF ORGANISM REACTIVITY AND MUCOSAL IMMUNITY IN MODULATING OF PATHOGENICITY AND VIRULENCE OF OPPORTUNISTIC MICROFLORA IN DYNAMICS OF INFECTIOUS PROCESS AND ALSO IN MACROAND MICROORGANISMS GENE POOLS MAINTENANCE (Роль реактивности организма и мукозальн
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Караулов Александр Викторович
Афанасьев Максим Станиславович
Несвижский Юрий Владимирович
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Инфекционные болезни |
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The review is summarizing for the first time the results of original research and literature data revealing the conditions of opportunistic microflora (OM) pathogenicity and virulence formation in the dynamics of the infectious process, as well as maintenance and formation of gene pools in host cells and microorganisms. It is established, that formation or loss of pathogenic and virulent properties of microorganisms in the body happens under the influence of its external environment, its overall physiological and immunological reactivity, mucosal immunity, as well as with the direct participation of horizontal gene transfer. Newly created microbial pathogens cause infectious-inflammatory diseases. However, acquired pathogenicity factors are lost after recovery. Plasticity of gene pools of the macroorganism and microorganisms allows owners of gene pools to respond adequately to changes in the external and internal body environment, improve and enhance overall and immunological reactivity of the macroorganism in ontogenesis, generate optimal for specific situations symbiotic or antagonistic relationships between them taking into account newly acquired or lost pathogenicity and virulence factors and form new phenotypic or genetic properties of microorganisms. Horizontal genetic transfer is the process of moving the genetic information which is possible between prokaryotic and eukaryotic cells both ways, as well as within a single cell.
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Публикация |
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Pro-neurogenic, Memory-Enhancing and Anti-stress Effects of DF302, a Novel Fluorine Gamma-Carboline Derivative with Multi-target Mechanism of Action
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Петер Леш
Стрекалова Т.В.
Умрюхин А.T.
Баженова Н.С.
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Molecular Neurobiology |
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A comparative study performed in mice investigating the action of DF302, a novel fluoride-containing gamma-carboline derivative, in comparison to the structurally similar neuroprotective drug dimebon. Drug effects on learning and memory, emotionality, hippocampal neurogenesis and mitochondrial functions, as well as AMPA-mediated currents and the 5-HT6 receptor are reported. In the step-down avoidance and fear-conditioning paradigms, bolus administration of drugs at doses of 10 or 40 mg/kg showed that only the higher dose of DF302 improved long-term memory while dimebon was ineffective at either dosage. Short-term memory and fear extinction remained unaltered across treatment groups. During the 5-day predation stress paradigm, oral drug treatment over a period of 2 weeks at the higher dosage regimen decreased anxiety-like behaviour. Both compounds supressed inter-male aggression in CD1 mice, the most eminent being the effects of DF302 in its highest dose. DF302 at the higher dose decreased floating behaviour in a 2-day swim test and after 21-day ultrasound stress. The density of Ki67-positive cells, a marker of adult neurogenesis, was reduced in the dentate gyrus of stressed dimebon-treated and non-treated mice, but not in DF302-treated mice. Non-stressed mice that received DF302 had a higher density of Ki67-positive cells than controls unlike dimebon-treated mice. Similar to dimebon, DF302 effectively potentiated AMPA receptor-mediated currents, bound to the 5-HT6 receptor, inhibited mitochondrial permeability transition and displayed cytoprotective properties in cellular models of neurodegeneration. Thus, DF302 exerts multi-target effects on the key mechanisms of neurodegenerative pathologies and can be considered as an optimized novel analogue of the neuroprotective agent dimebon.
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тезис
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How regularities of mortality statistics explain why we age despite having potentially ageless somatic stem cells
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Крутько Вячеслав Николаевич
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Biogerontology |
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Researchers working in the area of ageing have found numerous manifestations of this process at the molecular biological level, including DNA and protein damage, accumulation of metabolic by-products, lipids peroxidation, macromolecular cross-linking, non-enzymatic glycosylation, anti-oxidant/pro-oxidant misbalance, rising of pro-inflammatory cytokines, etc. This results in an increase in the proportion of cells in growth arrest, reduction of the rate of information processing, metabolic rate decrease, and decrease in rates of other processes characterizing dynamic aspects of the organism’s interaction with its environment. Such staggering multilevel diversity in manifestation of senescence precludes (without methodology of systems biology) development of a correct understanding of its primary causes and does not allow for developing approaches capable of postponing ageing or reducing organisms’ ageing rate to attain health preservation. Moreover, it turns out that damage production and damage elimination processes, the misbalance of which results in the ageing process, can to a large extent be regulated by external signals. The purpose of this report is to provide evidence supporting this view and its compatibility with the regularities of mortality statistics, because the main idea is very simple. Even potentially a non-senescent but certainly not immortal body must start to age under inadequate conditions (like a non-melting piece of ice taken out from the deepfreeze inevitably start to melt at the temperatures above zero Celsius). This conclusion is totally consistent with existing patterns of mortality and with agelessness potential of somatic stem cells. Therefore, there is no need to build up and explore too complicated, computational and sophisticated systems models of intrinsic ageing to understand the origin of this mainly extrinsic root cause of natural ageing, which is controlled by environmental signals. In our case, a simple phenomenological black-box approach with Input–Output analysis is ample. Here Input refers to the environmentally dependent initial force of mortality, whereas Output is a rate of age-related increase of mortality force.
Читать
тезис
Публикация |
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ROLE OF ORGANISM REACTIVITY AND MUCOSAL IMMUNITY IN MODULATING OF PATHOGENICITY AND VIRULENCE OF OPPORTUNISTIC MICROFLORA IN DYNAMICS OF INFECTIOUS PROCESS AND ALSO IN MACROAND MICROORGANISMS GENE POOLS MAINTENANCE (Роль реактивности организма и мукозальн
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Караулов Александр Викторович (Заведующий кафедрой)
Афанасьев Максим Станиславович (Профессор)
Несвижский Юрий Владимирович (Профессор)
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Инфекционные болезни |
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The review is summarizing for the first time the results of original research and literature data revealing the conditions of opportunistic microflora (OM) pathogenicity and virulence formation in the dynamics of the infectious process, as well as maintenance and formation of gene pools in host cells and microorganisms. It is established, that formation or loss of pathogenic and virulent properties of microorganisms in the body happens under the influence of its external environment, its overall physiological and immunological reactivity, mucosal immunity, as well as with the direct participation of horizontal gene transfer. Newly created microbial pathogens cause infectious-inflammatory diseases. However, acquired pathogenicity factors are lost after recovery. Plasticity of gene pools of the macroorganism and microorganisms allows owners of gene pools to respond adequately to changes in the external and internal body environment, improve and enhance overall and immunological reactivity of the macroorganism in ontogenesis, generate optimal for specific situations symbiotic or antagonistic relationships between them taking into account newly acquired or lost pathogenicity and virulence factors and form new phenotypic or genetic properties of microorganisms. Horizontal genetic transfer is the process of moving the genetic information which is possible between prokaryotic and eukaryotic cells both ways, as well as within a single cell.
Читать
тезис
Публикация |
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Pro-neurogenic, Memory-Enhancing and Anti-stress Effects of DF302, a Novel Fluorine Gamma-Carboline Derivative with Multi-target Mechanism of Action
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Петер Леш (руководитель лаборатории Психиатрической Нейробиологии)
Стрекалова Т.В. ( зам руководителя лаборатории Психиатрической Нейробиологии)
Умрюхин А.T. (старший научный сотрудник)
Баженова Н.С. (младший научный сотрудник)
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Molecular Neurobiology |
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A comparative study performed in mice investigating the action of DF302, a novel fluoride-containing gamma-carboline derivative, in comparison to the structurally similar neuroprotective drug dimebon. Drug effects on learning and memory, emotionality, hippocampal neurogenesis and mitochondrial functions, as well as AMPA-mediated currents and the 5-HT6 receptor are reported. In the step-down avoidance and fear-conditioning paradigms, bolus administration of drugs at doses of 10 or 40 mg/kg showed that only the higher dose of DF302 improved long-term memory while dimebon was ineffective at either dosage. Short-term memory and fear extinction remained unaltered across treatment groups. During the 5-day predation stress paradigm, oral drug treatment over a period of 2 weeks at the higher dosage regimen decreased anxiety-like behaviour. Both compounds supressed inter-male aggression in CD1 mice, the most eminent being the effects of DF302 in its highest dose. DF302 at the higher dose decreased floating behaviour in a 2-day swim test and after 21-day ultrasound stress. The density of Ki67-positive cells, a marker of adult neurogenesis, was reduced in the dentate gyrus of stressed dimebon-treated and non-treated mice, but not in DF302-treated mice. Non-stressed mice that received DF302 had a higher density of Ki67-positive cells than controls unlike dimebon-treated mice. Similar to dimebon, DF302 effectively potentiated AMPA receptor-mediated currents, bound to the 5-HT6 receptor, inhibited mitochondrial permeability transition and displayed cytoprotective properties in cellular models of neurodegeneration. Thus, DF302 exerts multi-target effects on the key mechanisms of neurodegenerative pathologies and can be considered as an optimized novel analogue of the neuroprotective agent dimebon.
Читать
тезис
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How regularities of mortality statistics explain why we age despite having potentially ageless somatic stem cells
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Крутько Вячеслав Николаевич (Профессор )
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Biogerontology |
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Researchers working in the area of ageing have found numerous manifestations of this process at the molecular biological level, including DNA and protein damage, accumulation of metabolic by-products, lipids peroxidation, macromolecular cross-linking, non-enzymatic glycosylation, anti-oxidant/pro-oxidant misbalance, rising of pro-inflammatory cytokines, etc. This results in an increase in the proportion of cells in growth arrest, reduction of the rate of information processing, metabolic rate decrease, and decrease in rates of other processes characterizing dynamic aspects of the organism’s interaction with its environment. Such staggering multilevel diversity in manifestation of senescence precludes (without methodology of systems biology) development of a correct understanding of its primary causes and does not allow for developing approaches capable of postponing ageing or reducing organisms’ ageing rate to attain health preservation. Moreover, it turns out that damage production and damage elimination processes, the misbalance of which results in the ageing process, can to a large extent be regulated by external signals. The purpose of this report is to provide evidence supporting this view and its compatibility with the regularities of mortality statistics, because the main idea is very simple. Even potentially a non-senescent but certainly not immortal body must start to age under inadequate conditions (like a non-melting piece of ice taken out from the deepfreeze inevitably start to melt at the temperatures above zero Celsius). This conclusion is totally consistent with existing patterns of mortality and with agelessness potential of somatic stem cells. Therefore, there is no need to build up and explore too complicated, computational and sophisticated systems models of intrinsic ageing to understand the origin of this mainly extrinsic root cause of natural ageing, which is controlled by environmental signals. In our case, a simple phenomenological black-box approach with Input–Output analysis is ample. Here Input refers to the environmentally dependent initial force of mortality, whereas Output is a rate of age-related increase of mortality force.
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тезис
Публикация |
