scholarly journals EMBRIOGENESIS OF NEURONAL ELENENTS (GLIOBLASTS AND GABAA RECEPTORS) IN THE HUMAN BRAIN NEUROIMMUNE SYSTEM UNDER PRENATAL ALCOHOL EXPOSURE

2021 ◽  
Vol 23 (4) ◽  
pp. 871-880
Author(s):  
T. V. Shushpanova ◽  
A. V. Solonsky ◽  
S. N. Shumilova ◽  
O. V. Shushpanova ◽  
N. A. Bokhan
Keyword(s):  
Human Brain ◽  
Glial Cells ◽  
Nervous Tissue ◽  
Benzodiazepine Receptors ◽  
Presynaptic Terminal ◽  
Human Embryos ◽  
Neuroimmune System ◽  
The Central Nervous System ◽  
Human Embryos And Fetuses ◽  
The Brain

Exposure to alcohol causes imbalances in neuroimmune function and impaired brain development. Alcohol activates the innate immune signaling pathways in the brain. Neuroimmune molecules expressed and secreted by glial cells of the brain (microglia, oligodendroglia) alter the function of neurons and further stimulate the development of alcoholic behavior. Various signaling pathways and brain cells are involved in the transmission of neuroimmune signals. Glial cells are the main sources of immune mediators in the brain, which respond to and release immune signals in the central nervous system. The aim of this study was to study neuronal elements: morphometric parameters of glioblasts, synaptic structures and properties of synaptosomal GABAA-benzodiazepine receptors of the neuroimmune system in the embryogenesis of the human brain under perinatal exposure to alcohol. Changes in glioblasts in the brain tissue of human embryos and fetuses were revealed under conditions of chronic prenatal alcoholization with an increase in gestational age compared with control subgroups: a significant increase in the average number of glioblasts, the length of the perimeters of presynaptic terminal structures, postsynaptic density, presynaptic terminal regions were significantly less (p < 0.01) in the study group than in the control comparison group. Exposure to ethanol leads to a decrease in the affinity of GABAA-benzodiazepine receptors, which affects neuronal plasticity associated with the development and differentiation of progenitor cells (glioblasts and neuroblasts) during embryogenesis of the human brain and leads to suppression of GABAergic function in the brain. This causes a disruption in the interconnection of embryonic cells in the brain, leads to excessive apoptosis due to the activation of glial cells of the nervous tissue, disruption of neuroimmune function in the developing brain, changes in neuronal circuits, as well as a change in the balance of excitatory and inhibitory effects, which affects the functional activity in the central nervous system. Glial activation is a compensatory reaction caused by neuroplastic changes aimed at adapting the developing brain of the embryo and fetus under conditions of neurotoxicity and hypoxia under the influence of prenatal alcoholization of the maternal organism and the effect of ethanol on the fetus. The dynamics of changes in glial elements and receptor activity in the nervous tissue of human embryos and fetuses under conditions of prenatal exposure to alcohol indicates a more pronounced effect of alcohol on the earliest stages of human embryo development, which is of great practical importance in planning pregnancy and the inadmissibility of alcoholization of the mother in order to avoid negative consequences in offspring. 

scholarly journals Embryology of the Human Brain

2008 ◽  
Vol 2 (3) ◽  
pp. 1-8
Author(s):  
Kohei Shiota
Keyword(s):  
Nervous System ◽  
Human Brain ◽  
Environmental Effects ◽  
Developing Brain ◽  
Human Embryos ◽  
Cns Development ◽  
The Third ◽  
Long Period ◽  
Human Embryos And Fetuses ◽  
The Brain

Abstract In this paper, the process of CNS development in human embryos and fetuses is described. The primordium of the nervous system appears as early as during the third week after fertilization, but its differentiation and maturation require a considerably long period of time until after birth. Therefore, the developing brain is vulnerable to various kinds of deleterious environmental effects during the preand perinatal life. This paper aims at giving an overview of the major organogenesis of the brain in human embryos and fetuses.

scholarly journals The Microbiota–Gut–Brain Axis and Alzheimer Disease. From Dysbiosis to Neurodegeneration: Focus on the Central Nervous System Glial Cells

2021 ◽  
Vol 10 (11) ◽  
pp. 2358
Author(s):  
Maria Grazia Giovannini ◽  
Daniele Lana ◽  
Chiara Traini ◽  
Maria Giuliana Vannucchi
Keyword(s):  
Alzheimer Disease ◽  
Glial Cells ◽  
Cell Types ◽  
The Past ◽  
The Central Nervous System ◽  
Diseased State ◽  
The Brain ◽  
Alzheimer Disease Pathogenesis ◽  
Brain Homeostasis

The microbiota–gut system can be thought of as a single unit that interacts with the brain via the “two-way” microbiota–gut–brain axis. Through this axis, a constant interplay mediated by the several products originating from the microbiota guarantees the physiological development and shaping of the gut and the brain. In the present review will be described the modalities through which the microbiota and gut control each other, and the main microbiota products conditioning both local and brain homeostasis. Much evidence has accumulated over the past decade in favor of a significant association between dysbiosis, neuroinflammation and neurodegeneration. Presently, the pathogenetic mechanisms triggered by molecules produced by the altered microbiota, also responsible for the onset and evolution of Alzheimer disease, will be described. Our attention will be focused on the role of astrocytes and microglia. Numerous studies have progressively demonstrated how these glial cells are important to ensure an adequate environment for neuronal activity in healthy conditions. Furthermore, it is becoming evident how both cell types can mediate the onset of neuroinflammation and lead to neurodegeneration when subjected to pathological stimuli. Based on this information, the role of the major microbiota products in shifting the activation profiles of astrocytes and microglia from a healthy to a diseased state will be discussed, focusing on Alzheimer disease pathogenesis.

Urea transport in the central nervous system

1962 ◽  
Vol 203 (4) ◽  
pp. 739-747 ◽  
Author(s):  
Charles R. Kleeman ◽  
Hugh Davson ◽  
Emanuel Levin
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Nervous Tissue ◽  
Urea Transport ◽  
Major Barrier ◽  
Rate Of Penetration ◽  
The Central Nervous System ◽  
Kinetics Of ◽  
The Brain ◽  
State Content

The kinetics of urea transport in the central nervous system have been studied in rabbits during sustained intravenous and intracisternal infusions of C12 and C14 urea. The steady state content of urea in the water phase of the white matter and cord was approximately equal to its content in plasma water. However, the water of whole brain and gray matter had levels of urea which exceeded those in plasma by 7 and 18%, respectively, whereas the urea in cerebrospinal fluid (CSF) was only 78% of the plasma level. Its rate of penetration into nervous tissue was approximately one-tenth as rapid as into muscle. The intravenous infusion of urea caused a significant decrease in water content of the brain and cord. It was estimated that urea infused into the subarachnoid space penetrated the central nervous system (CNS) tissues at four to five times the rate of transport from blood to CNS tissues. These studies suggest that intravenous infusions of urea lower CSF pressure by decreasing the volume of the brain and cord. The major barrier to urea penetration into nervous tissue is at the capillary level, and not the plasma membrane of the glial or neuronal cells.

Experiments on the ‘Overgrowth’ Phenomenon in the Brain of Chick Embryos

Development ◽  
1959 ◽  
Vol 7 (2) ◽  
pp. 122-127
Author(s):  
Harry Bergquist
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Neural Tube ◽  
Human Embryos ◽  
Chick Embryos ◽  
Cranial Cavity ◽  
The Central Nervous System ◽  
The Brain ◽  
Rostral Part ◽  
Exact Term

Patten (1952) described ‘a curious distortion of the central nervous system’ in human embryos measuring 5, 7, 12·5, 20, and 30 mm. in length, as well as in some pig embryos. The malformation was called ‘overgrowth of the neural tube’. Instead of the indecisive word ‘overgrowth’ the present writer suggests the more exact term ‘hypermorphosis’ should be used for this malformation. Patten described it in the following way: ‘the neural tube epithelium had started to grow wildly so that it became folded, and refolded on itself, as if it was crowded into a cranial space fairly normal in size and shape’. The phenomenon was most distinctly developed in the rostral part of the neural tube. In some cases the cranial cavity was expanded by the process, giving rise to a high-crowned skull. In other cases an encephalocoel was formed. In later papers (1953, 1957) Patten discussed this phenomenon further.

The Benzodiazepine Receptor in Normal and Pathological Human Brain

1978 ◽  
Vol 133 (3) ◽  
pp. 261-268 ◽  
Author(s):  
H. Möhler ◽  
T. Okada
Keyword(s):  
Central Nervous System ◽  
Membrane Fraction ◽  
Benzodiazepine Receptors ◽  
Benzodiazepine Receptor ◽  
Synaptic Membrane ◽  
Huntington's Chorea ◽  
High Affinity ◽  
Cortical Areas ◽  
The Central Nervous System ◽  
The Brain

SummaryBenzodiazepines bind with high affinity to a specific benzodiazepine receptor, which occurs exclusively in the central nervous system. The affinity of various benzodiazepines to the receptor closely parallels their pharmacological and therapeutic potency. Binding to the receptor is stereospecific. The receptor is mainly localized in the synaptic membrane fraction and has its highest density in cortical areas of the brain. In Huntington's chorea a decrease in benzodiazepine receptor binding is found in caudate nucleus and putamen, which, at least in putamen, is due to a loss of benzodiazepine receptors apparently located on GABA neurones, which degenerate in Huntington's chorea. The loss of benzodiazepine receptors might explain why the ameliorative effects of benzodiazepines in the early stages of the disease are not sustained in the later stages.

scholarly journals Dehydration-Induced Anorexia Reduces Astrocyte Density in the Rat Corpus Callosum

2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Daniel Reyes-Haro ◽  
Francisco Emmanuel Labrada-Moncada ◽  
Ricardo Miledi ◽  
Ataúlfo Martínez-Torres
Keyword(s):  
Food Intake ◽  
Corpus Callosum ◽  
Glial Cell ◽  
Cell Density ◽  
Glial Cells ◽  
The Body ◽  
The Central Nervous System ◽  
The Brain ◽  
Cell Somata ◽  
Core Features

Anorexia nervosa is an eating disorder associated with severe weight loss as a consequence of voluntary food intake avoidance. Animal models such as dehydration-induced anorexia (DIA) mimic core features of the disorder, including voluntary reduction in food intake, which compromises the supply of energy to the brain. Glial cells, the major population of nerve cells in the central nervous system, play a crucial role in supplying energy to the neurons. The corpus callosum (CC) is the largest white matter tract in mammals, and more than 99% of the cell somata correspond to glial cells in rodents. Whether glial cell density is altered in anorexia is unknown. Thus, the aim of this study was to estimate glial cell density in the three main regions of the CC (genu, body, and splenium) in a murine model of DIA. The astrocyte density was significantly reduced (~34%) for the DIA group in the body of the CC, whereas in the genu and the splenium no significant changes were observed. DIA and forced food restriction (FFR) also reduced the ratio of astrocytes to glial cells by 57.5% and 22%, respectively, in the body of CC. Thus, we conclude that DIA reduces astrocyte density only in the body of the rat CC.

The Ferrier Lecture, 1968 - Motor apparatus of the baboon’s hand

1969 ◽  
Vol 173 (1031) ◽  
pp. 141-174 ◽  
Keyword(s):  
Nervous System ◽  
Human Brain ◽  
Medical Director ◽  
Lunatic Asylum ◽  
Cerebral Lesions ◽  
The West ◽  
Experimental Proof ◽  
Bony Landmarks ◽  
The Central Nervous System ◽  
The Brain

It is exactly 40 years since Ferrier died, and 39 years since Sherrington gave the first Ferrier Lecture in honour of his work. Sherrington (1906) had dedicated The integrative action of the nervous system to Ferrier ‘in token of recognition of his many services to the experimental physiology of the central nervous system’. At Aberdeen Ferrier had been taught by Bain, the Professor of Logic, who kept a model of the human brain upon his lecture table. Ferrier moved to London in 1870, and was excited by Hughlings Jackson’s revolutionary discoveries and ideas about the nature and localization of the sensory and motor functions of the human brain. Early in 1873 he discussed Fritsch & Hitzig’s (1870) pioneer galvanic stimulations of the dog’s cortex with his friend James Crichton-Browne. In the spring and summer of that year he performed his pioneer faradic stimulations of the brains of monkeys in the laboratory of the West Riding Lunatic Asylum, of which Crichton-Browne was Medical Director (Sherrington 1928). He sought to ‘put to experimental proof the views entertained by Dr Hughlings Jackson on the pathology of Epilepsy, Chorea and Hemiplegia, by imitating artificially the "destroying" and “discharging lesions” of disease which his writings have defined and differentiated’ (Ferrier 1873). 'The phenomena of localized and unilateral convulsive movements, depending, as Hughlings Jackson shows, on vital irritation of certain regions of the cortex, are essentially of the same nature as those caused by electrisation of the same regions’ (1876, p. 133). But Ferrier believed that many of the movements he mapped by electrical stimulation had evidently a purposive or volitional character’ (1876, p. 163). In 1876 he transferred his monkey map to the brain of man, and described of the relation between brain fissures and bony landmarks; and in 1883 he suggested that the time had come when localized cerebral lesions should be excised by the surgeon. For this, as he later recalled with amusement, he was criticized in an editorial in the Lancet (Ferrier, 1888), but in 1884 Godlee removed a localized tumour ‘of the size of a walnut’ (Sherrington 1928) from the Rolandic cortex through an opening exactly overlying it and but little larger than itself. Ferrier and Hughlings Jackson both witnessed this memorable operation (Trotter 1934). As time went on, experimentalists interested themselves more in defining details of localization than in developing concepts of function (Phillips 1966). ‘More penetrative modes and aims of analysis came to be little pursued,’ wrote Sherrington (1928). ‘A localization vogue reigned for nearly a quarter of a century, and became in due course tedious and relatively infertile.’

scholarly journals The Serendipity of Viral Trans-Neuronal Specificity: More Than Meets the Eye

2021 ◽  
Vol 15 ◽  
Author(s):  
Kevin Thomas Beier
Keyword(s):  
Glial Cells ◽  
Brain Parenchyma ◽  
Synaptic Connections ◽  
Widespread Application ◽  
Host Immune Responses ◽  
The Central Nervous System ◽  
One Step ◽  
Neuronal Specificity ◽  
The Brain ◽  
Neuroscience Community

Trans-neuronal viruses are frequently used as neuroanatomical tools for mapping neuronal circuits. Specifically, recombinant one-step rabies viruses (RABV) have been instrumental in the widespread application of viral circuit mapping, as these viruses have enabled labs to map the direct inputs onto defined cell populations. Within the neuroscience community, it is widely believed that RABV spreads directly between neurons via synaptic connections, a hypothesis based principally on two observations. First, the virus labels neurons in a pattern consistent with known anatomical connectivity. Second, few glial cells appear to be infected following RABV injections, despite the fact that glial cells are abundant in the brain. However, there is no direct evidence that RABV can actually be transmitted through synaptic connections. Here we review the immunosubversive mechanisms that are critical to RABV’s success for infiltration of the central nervous system (CNS). These include interfering with and ultimately killing migratory T cells while maintaining levels of interferon (IFN) signaling in the brain parenchyma. Finally, we critically evaluate studies that support or are against synaptically-restricted RABV transmission and the implications of viral-host immune responses for RABV transmission in the brain.

Regulating Systems in Neuroimmunology

2021 ◽  
Author(s):  
William H. Walker II ◽  
A. Courtney DeVries
Keyword(s):  
Nervous System ◽  
Immune System ◽  
Scientific Investigation ◽  
Neuroimmune System ◽  
Disease States ◽  
Behavioral Abnormalities ◽  
Optimal Health ◽  
The Central Nervous System ◽  
Active Research ◽  
The Brain

Neuroimmunology is the study of the interaction between the immune system and nervous system during development, homeostasis, and disease states. Descriptions of neuroinflammatory diseases dates back centuries. However, in depth scientific investigation in the field began in the late 19th century and continues into the 21st century. Contrary to prior dogma in the field of neuroimmunology, there is immense reciprocal crosstalk between the brain and the immune system throughout development, homeostasis, and disease states. Proper neuroimmune functioning is necessary for optimal health, as the neuroimmune system regulates vital processes including neuronal signaling, synapse pruning, and clearance of debris and pathogens within the central nervous system. Perturbations in optimal neuroimmune functioning can have detrimental consequences for the host and underlie a myriad of physical, cognitive, and behavioral abnormalities. As such, the field of neuroimmunology is still relatively young and dynamic and represents an area of active research and discovery.

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