scholarly journals The Mechanisms Underlying the Protective Action of Selenium Nanoparticles against Ischemia/Reoxygenation Are Mediated by the Activation of the Ca2+ Signaling System of Astrocytes and Reactive Astrogliosis

2021 ◽  
Vol 22 (23) ◽  
pp. 12825
Author(s):  
Elena G. Varlamova ◽  
Egor A. Turovsky ◽  
Valentina A. Babenko ◽  
Egor Y. Plotnikov
Keyword(s):  
Cerebral Cortex ◽  
Protective Action ◽  
Selenium Nanoparticles ◽  
Ip3 Receptor ◽  
Extracellular Medium ◽  
Phosphoinositide Signaling ◽  
Anticancer Effects ◽  
Paracrine Activation ◽  
First Time ◽  
The Brain

In recent years, much attention has been paid to the study of the therapeutic effect of the microelement selenium, its compounds, especially selenium nanoparticles, with a large number of works devoted to their anticancer effects. Studies proving the neuroprotective properties of selenium nanoparticles in various neurodegenerative diseases began to appear only in the last 5 years. Nevertheless, the mechanisms of the neuroprotective action of selenium nanoparticles under conditions of ischemia and reoxygenation remain unexplored, especially for intracellular Ca2+ signaling and neuroglial interactions. This work is devoted to the study of the cytoprotective mechanisms of selenium nanoparticles in the neuroglial networks of the cerebral cortex under conditions of ischemia/reoxygenation. It was shown for the first time that selenium nanoparticles dose-dependently induce the generation of Ca2+ signals selectively in astrocytes obtained from different parts of the brain. The generation of these Ca2+ signals by astrocytes occurs through the release of Ca2+ ions from the endoplasmic reticulum through the IP3 receptor upon activation of the phosphoinositide signaling pathway. An increase in the concentration of cytosolic Ca2+ in astrocytes leads to the opening of connexin Cx43 hemichannels and the release of ATP and lactate into the extracellular medium, which trigger paracrine activation of the astrocytic network through purinergic receptors. Incubation of cerebral cortex cells with selenium nanoparticles suppresses ischemia-induced increase in cytosolic Ca2+ and necrotic cell death. Activation of A2 reactive astrocytes exclusively after ischemia/reoxygenation, a decrease in the expression level of a number of proapoptotic and proinflammatory genes, an increase in lactate release by astrocytes, and suppression of the hyperexcitation of neuronal networks formed the basis of the cytoprotective effect of selenium nanoparticles in our studies.

Coenzymes Q9 and Q10, Vitamin E and Peroxidation in Rat Synaptic and Non-Synaptic Occipital Cerebral Cortex Mitochondria during Ageing

2001 ◽  
Vol 382 (6) ◽  
pp. 925-931 ◽  
Author(s):  
Maurizio Battino ◽  
Stefano Bompadre ◽  
Luciana Leone ◽  
Roberto F. Villa ◽  
Antonella Gorini
Keyword(s):  
Cerebral Cortex ◽  
Vitamin E ◽  
Coenzyme Q ◽  
Direct Injection ◽  
Extraction Procedure ◽  
Brain Mitochondria ◽  
Membrane Structures ◽  
First Time ◽  
The Brain

Abstract Great attention has been devoted both to ageing phenomena at the mitochondrial level and to the antioxidant status of membrane structures. These kinds of investigations are difficult to perform in the brain because of its heterogeneity. It is known that synaptic heavy mitochondria (HM) may represent an aged mitochondrial population characterized by a partial impairment of their typical mitochondrial function. We arranged a novel system requiring no extraction procedure, very limited handling of the samples and their direct injection into the HPLC apparatus, to carry out, for the first time, a systematic and concomitant determination of vitamin E, Coenzyme Q[9] (CoQ[9]) and Coenzyme Q[10] (CoQ[10]) contents in rat brain mitochondria. The trends found for CoQ[9] and CoQ[10] levels in synaptic and nonsynaptic occipital cerebral cortex mitochondria during rat ageing are consistent with previous data. Hydroperoxides (HP) differed with age and it was confirmed that in the HM fraction the summation of contributions results in an oxidatively jeopardized subpopulation. We found that vitamin E seems to increase with age, at least in nonsynaptic free (FM) and synaptic light (LM) mitochondria, while it was inclined to remain substantially constant in HM.

scholarly journals Mechanism of Ca2+-Dependent Pro-Apoptotic Action of Selenium Nanoparticles, Mediated by Activation of Cx43 Hemichannels

Biology ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 743
Author(s):  
Egor A. Turovsky ◽  
Elena G. Varlamova
Keyword(s):  
Intracellular Signaling ◽  
Cell Activation ◽  
Selenium Nanoparticles ◽  
Ip3 Receptor ◽  
Glioblastoma Cells ◽  
Vesicular Release ◽  
Induction Of Apoptosis ◽  
Relationship Of ◽  
First Time

To date, there are practically no data on the mechanisms of the selenium nanoparticles action on calcium homeostasis, intracellular signaling in cancer cells, and on the relationship of signaling pathways activated by an increase in Ca2+ in the cytosol with the induction of apoptosis, which is of great importance. The study of these mechanisms is important for understanding the cytotoxic effect of selenium nanoparticles and the role of this microelement in the regulation of carcinogenesis. The work is devoted to the study of the role of selenium nanoparticles obtained by laser ablation in the activation of the calcium signaling system and the induction of apoptosis in human glioblastoma cells (A-172 cell line). In this work, it was shown for the first time that the generation of Ca2+ signals in A-172 cells occurs in response to the application of various concentrations of selenium nanoparticles. The intracellular mechanism responsible for the generation of these Ca2+ signals has also been established. It was found that nanoparticles promote the mobilization of Ca2+ ions from the endoplasmic reticulum through the IP3-receptor. This leads to the activation of vesicular release of ATP through connexin hemichannels (Cx43) and paracrine cell activation through purinergic receptors (mainly P2Y). In addition, it was shown that the activation of this signaling pathway is accompanied by an increase in the expression of pro-apoptotic genes and the induction of apoptosis. For the first time, the role of Cx43 in the regulation of apoptosis caused by selenium nanoparticles in glioblastoma cells has been shown. It was found that inhibition of Cx43 leads to a significant suppression of the induction of apoptosis in these cells after 24 h treatment of cells with selenium nanoparticles at a concentration of 5 µg/mL.

scholarly journals Effects of ergotamine on the central nervous system using untargeted metabolomics analysis in a mouse model

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Priyanka Reddy ◽  
Delphine Vincent ◽  
Joanne Hemsworth ◽  
Vilnis Ezernieks ◽  
Kathryn Guthridge ◽  
...  
Keyword(s):  
Cerebral Cortex ◽  
Ergot Alkaloid ◽  
Post Partum ◽  
Economic Importance ◽  
Parasitic Fungus ◽  
Claviceps Purpurea ◽  
Metabolomic Profiling ◽  
The Central Nervous System ◽  
First Time ◽  
The Brain

AbstractThe ergot alkaloid ergotamine is produced by Claviceps purpurea, a parasitic fungus that commonly infects crops and pastures of high agricultural and economic importance. In humans and livestock, symptoms of ergotism include necrosis and gangrene, high blood pressure, heart rate, thermoregulatory dysfunction and hallucinations. However, ergotamine is also used in pharmaceutical applications to treat migraines and stop post-partum hemorrhage. To define its effects, metabolomic profiling of the brain was undertaken to determine pathways perturbed by ergotamine treatment. Metabolomic profiling identified the brainstem and cerebral cortex as regions with greatest variation. In the brainstem, dysregulation of the neurotransmitter epinephrine, and the psychoactive compound 2-arachidonylglycerol was identified. In the cerebral cortex, energy related metabolites isobutyryl-L-carnitine and S-3-oxodecanoyl cysteamine were affected and concentrations of adenylosuccinate, a metabolite associated with mental retardation, were higher. This study demonstrates, for the first time, key metabolomic pathways involved in the behavioural and physiological dysfunction of ergot alkaloid intoxicated animals.

Glucuronyl 3-sulfate occurs exclusively on distal unmyelinated terminals of selected sensory neurons in the peripheral nervous system

1995 ◽  
Vol 53 ◽  
pp. 958-959
Author(s):  
S.S. Spicer ◽  
B.A. Schulte
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Cerebral Cortex ◽  
Peripheral Nervous System ◽  
Sensory Neurons ◽  
Sensory Nerves ◽  
Tissue Antigens ◽  
The Central Nervous System ◽  
The Brain ◽  
Leu 7

Generation of monoclonal antibodies (MAbs) against tissue antigens has yielded several (VC1.1, HNK- 1, L2, 4F4 and anti-leu 7) which recognize the unique sugar epitope, glucuronyl 3-sulfate (Glc A3- SO4). In the central nervous system, these MAbs have demonstrated Glc A3-SO4 at the surface of neurons in the cerebral cortex, the cerebellum, the retina and other widespread regions of the brain.Here we describe the distribution of Glc A3-SO4 in the peripheral nervous system as determined by immunostaining with a MAb (VC 1.1) developed against antigen in the cat visual cortex. Outside the central nervous system, immunoreactivity was observed only in peripheral terminals of selected sensory nerves conducting transduction signals for touch, hearing, balance and taste. On the glassy membrane of the sinus hair in murine nasal skin, just deep to the ringwurt, VC 1.1 delineated an intensely stained, plaque-like area (Fig. 1). This previously unrecognized structure of the nasal vibrissae presumably serves as a tactile end organ and to our knowledge is not demonstrable by means other than its selective immunopositivity with VC1.1 and its appearance as a densely fibrillar area in H&E stained sections.

Neurotransmitter systems of female mouse brain during growth of malignant melanoma modeled on the background of chronic pain

2018 ◽  
pp. 49-55
Author(s):  
О.И. Кит ◽  
И.М. Котиева ◽  
Е.М. Франциянц ◽  
И.В. Каплиева ◽  
Л.К. Трепитаки ◽  
...  
Keyword(s):  
Chronic Pain ◽  
Cerebral Cortex ◽  
Malignant Melanoma ◽  
Sciatic Nerve ◽  
Female Mouse ◽  
Combined Effects ◽  
Malignant Growth ◽  
Course Of Disease ◽  
The Brain ◽  
Melanoma Growth

Известно, что биогенные амины (БА) участвуют в злокачественном росте, их уровень изменяется в ЦНС при болевом воздействии, однако исследований о сочетанном влиянии хронической боли (ХБ) и онкопатологии на динамику БА в головном мозге не проводилось. Цель: изучить особенности баланса БА в коре головного мозга в динамике роста меланомы, воспроизведенной на фоне ХБ. Материалы и методы. Работа выполнена на 64 мышах-самках, весом 21-22 г. Животным основной группы меланому В16/F10 перевивали под кожу спины через 2 недели после перевязки седалищных нервов. Группой сравнения служили мыши с меланомой без боли. Уровни БА: адреналина, норадреналина, дофамина (ДА), серотонина (5-НТ), гистамина, а также 5-ОИУК определяли методом иммуноферментного анализа. Результаты. У мышей с ХБ уменьшается содержание большинства БА, однако уровень ДА не изменяется. Метаболизм 5-НТ происходит с участием МАО. Развитие меланомы сопровождается увеличением содержания ДА и 5-НТ, тогда как МАО - ингибируется. Направленность сдвигов БА при развитии меланомы на фоне ХБ оказалась практически такой же, как и без неё. В то же время ХБ ограничивает накопление 5-НТ в коре мозга при меланоме, что сопровождается более агрессивным её течением. Выводы. ХБ ограничивает включение стресс-лимитирующих механизмов в головном мозге при развитии меланомы у мышей, что приводит к более агрессивному течению злокачественного процесса. Biogenic amines (BA) are known to be involved in malignant growth, and their CNS levels change in pain; however, there are no studies of combined effects of chronic pain (CP) and cancer on BA dynamics in the brain. Aim: To study features of BA balance in the cerebral cortex during melanoma growth associated with CP. Material and methods. The study included 64 female mice weighing 21-22 g. In the main groups, B16/F10 melanoma was transplanted under the skin of the back two weeks following sciatic nerve ligation. Mice with melanoma without pain were used as the control. Concentrations of BA: adrenaline, noradrenaline, dopamine (DA), serotonin (5-HT), histamine and 5-HIAA were measured with ELISA. Results. Concentrations of BAs decreased in mice with CP although DA levels did not change. 5-HT metabolism involved MAO. The development of melanoma was accompanied by increases in DA and 5-HT whereas MAO was inhibited. The direction of BA changes during the development of melanoma was the same with and without CP. At the same time, CP with melanoma limited accumulation of 5-HT in the cerebral cortex, which resulted in even more aggressive course of cancer. Conclusion. CP restricted the activation of cerebral stress-limiting mechanisms during the development of melanoma in mice, which resulted in a more aggressive course of disease.

Information-based decoding of the coupling among human brain activity and movement paths

2021 ◽  
pp. 1-10
Author(s):  
Shahul Mujib Kamal ◽  
Norazryana Mat Dawi ◽  
Hamidreza Namazi
Keyword(s):  
Brain Activity ◽  
Point Of View ◽  
Physiological Signals ◽  
Human Walking ◽  
Eeg Signals ◽  
Rehabilitation Science ◽  
Information Contents ◽  
First Time ◽  
The Brain ◽  
Brain Reaction

BACKGROUND: Walking like many other actions of a human is controlled by the brain through the nervous system. In fact, if a problem occurs in our brain, we cannot walk correctly. Therefore, the analysis of the coupling of brain activity and walking is very important especially in rehabilitation science. The complexity of movement paths is one of the factors that affect human walking. For instance, if we walk on a path that is more complex, our brain activity increases to adjust our movements. OBJECTIVE: This study for the first time analyzed the coupling of walking paths and brain reaction from the information point of view. METHODS: We analyzed the Shannon entropy for electroencephalography (EEG) signals versus the walking paths in order to relate their information contents. RESULTS: According to the results, walking on a path that contains more information causes more information in EEG signals. A strong correlation (p= 0.9999) was observed between the information contents of EEG signals and walking paths. Our method of analysis can also be used to investigate the relation among other physiological signals of a human and walking paths, which has great benefits in rehabilitation science.

scholarly journals Long-Term Glucose Starvation Induces Inflammatory Responses and Phenotype Switch in Primary Cortical Rat Astrocytes

2021 ◽  
Author(s):  
Vanessa Kogel ◽  
Stefanie Trinh ◽  
Natalie Gasterich ◽  
Cordian Beyer ◽  
Jochen Seitz
Keyword(s):  
Cerebral Cortex ◽  
Synapse Formation ◽  
Inflammatory Responses ◽  
Glucose Starvation ◽  
Unfolded Protein ◽  
Genes Encoding ◽  
Phenotype Switch ◽  
The Unfolded Protein Response ◽  
The Brain

AbstractAstrocytes are the most abundant cell type in the brain and crucial to ensure the metabolic supply of neurons and their synapse formation. Overnutrition as present in patients suffering from obesity causes astrogliosis in the hypothalamus. Other diseases accompanied by malnutrition appear to have an impact on the brain and astrocyte function. In the eating disorder anorexia nervosa (AN), patients suffer from undernutrition and develop volume reductions of the cerebral cortex, associated with reduced astrocyte proliferation and cell count. Although an effect on astrocytes and their function has already been shown for overnutrition, their role in long-term undernutrition remains unclear. The present study used primary rat cerebral cortex astrocytes to investigate their response to chronic glucose starvation. Cells were grown with a medium containing a reduced glucose concentration (2 mM) for 15 days. Long-term glucose starvation increased the expression of a subset of pro-inflammatory genes and shifted the primary astrocyte population to the pro-inflammatory A1-like phenotype. Moreover, genes encoding for proteins involved in the unfolded protein response were elevated. Our findings demonstrate that astrocytes under chronic glucose starvation respond with an inflammatory reaction. With respect to the multiple functions of astrocytes, an association between elevated inflammatory responses due to chronic starvation and alterations found in the brain of patients suffering from undernutrition seems possible.

THE METABOLISM OF NORMAL BRAIN AND HUMAN GLIOMAS IN RELATION TO CELL TYPE AND DENSITY

1955 ◽  
Vol 33 (3) ◽  
pp. 395-403 ◽  
Author(s):  
Irving H. Heller ◽  
K. A. C. Elliott
Keyword(s):  
Cerebral Cortex ◽  
White Matter ◽  
Brain Tumors ◽  
Corpus Callosum ◽  
Oxygen Uptake ◽  
Glial Cells ◽  
Cerebellar Cortex ◽  
Unit Weight ◽  
Uptake Rates ◽  
The Brain

Per unit weight, cerebral and cerebellar cortex respire much more actively than corpus callosum. The rate per cell nucleus is highest in cerebral cortex, lower in corpus callosum, and still lower in cerebellar cortex. The oxygen uptake rates of the brain tumors studied, with the exception of an oligodendroglioma, were about the same as that of white matter on the weight basis but lower than that of cerebral cortex or white matter on the cell basis. In agreement with previous work, an oligodendroglioma respired much more actively than the other tumors. The rates of glycolysis of the brain tumors per unit weight were low but, relative to their respiration rate, glycolysis was higher than in normal gray or white matter. Consideration of the figures obtained leads to the following tentative conclusions: Glial cells of corpus callosum respire more actively than the neurons of the cerebellar cortex. Neurons of the cerebral cortex respire on the average much more actively than neurons of the cerebellar cortex or glial cells. Considerably more than 70% of the oxygen uptake by cerebral cortex is due to neurons. The oxygen uptake rates of normal oligodendroglia and astrocytes are probably about the same as the rates found per nucleus in an oligodendroglioma and in astrocytomas; oligodendroglia respire much more actively than astrocytes.

Dream Bizarreness as the Cognitive Correlate of Altered Neuronal Behavior in REM Sleep

1989 ◽  
Vol 1 (3) ◽  
pp. 201-222 ◽  
Author(s):  
Adam N. Mamelak ◽  
J. Allan Hobson
Keyword(s):  
Neural Networks ◽  
Cerebral Cortex ◽  
Rem Sleep ◽  
Neuronal Dynamics ◽  
Neurophysiological Model ◽  
The Relationship ◽  
Cognitive Feature ◽  
The Brain ◽  
Cognitive Correlate ◽  
Raphe Neurons

Bizarreness is a cognitive feature common to REM sleep dreams, which can be easily measured. Because bizarreness is highly specific to dreaming, we propose that it is most likely brought about by changes in neuronal activity that are specific to REM sleep. At the level of the dream plot, bizarreness can be defined as either discontinuity or incongruity. In addition, the dreamer's thoughts about the plot may be logically deficient. We propose that dream bizarreness is the cognitive concomitant of two kinds of changes in neuronal dynamics during REM sleep. One is the disinhibition of forebrain networks caused by the withdrawal of the modulatory influences of norepinephrine (NE) and serotonin (5HT) in REM sleep, secondary to cessation of firing of locus coeruleus and dorsal raphe neurons. This aminergic demodulation can be mathematically modeled as a shift toward increased error at the outputs from neural networks, and these errors might be represented cognitively as incongruities and/or discontinuities. We also consider the possibility that discontinuities are the cognitive concomitant of sudden bifurcations or “jumps” in the responses of forebrain neuronal networks. These bifurcations are caused by phasic discharge of pontogeniculooccipital (PGO) neurons during REM sleep, providing a source of cholinergic modulation to the forebrain which could evoke unpredictable network responses. When phasic PGO activity stops, the resultant activity in the brain may be wholly unrelated to patterns of activity dominant before such phasic stimulation began. Mathematically such sudden shifts from one pattern of activity to a second, unrelated one is called a bifurcation. We propose that the neuronal bifurcations brought about by PGO activity might be represented cognitively as bizarre discontinuities of dream plot. We regard these proposals as preliminary attempts to model the relationship between dream cognition and REM sleep neurophysiology. This neurophysiological model of dream bizarreness may also prove useful in understanding the contributions of REM sleep to the developmental and experiential plasticity of the cerebral cortex.

Normal ageing and the brain

1998 ◽  
Vol 15 (1) ◽  
pp. 26-28
Author(s):  
CS Breathnach
Keyword(s):  
Cerebral Cortex ◽  
Imaging Techniques ◽  
Structure And Function ◽  
Ageing Population ◽  
Cell Shrinkage ◽  
Ageing Processes ◽  
Normal Ageing ◽  
And Function ◽  
Ageing Brain ◽  
The Brain

AbstractInterest in the psychiatric aspects of old age predated the institution of geriatrics as a clinical discipline, but the systematic study of the ageing brain only began in the second half of this century when an ageing population presented a global numerical challenge to society. In the senescent cerebral cortex, though the number of neurons is not reduced, cell shrinkage results in synaptic impoverishment with consequent cognitive impairment. Recent advances in imaging techniques, combined with burgeoning knowledge of neurobiological structure and function, have increased our understanding of the ageing processes in the human brain and permit an optimistic approach in the application of the newer insights into neuropsychology and geriatric psychiatry.

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