Letter to the Editor

PEDIATRICS ◽  
1994 ◽  
Vol 93 (1) ◽  
pp. 156-156
Author(s):  
Thor Willy Ruud Hansen
Keyword(s):  
Nervous System ◽  
Glial Cells ◽  
Experimental Designs ◽  
Research Experience ◽  
Relevant Research ◽  
The Past ◽  
Letter To The Editor ◽  
Limited Scope

Dr Aschner has some very interesting comments on the role of glial cells in bilirubin neurotoxicity. His suggestion that bilirubin researchers should focus some of their interest on this group of cells, given the increase in knowledge about their more complex role in nervous system homeostasis, is well taken. It would certainly be quite welcome if investigators with relevant research experience would include bilirubin in their future experimental designs. It seems appropriate in this context to mention the fact that bilirubin researchers in the past have given attention to glial cells, although perhaps with a more limited scope than that suggested by Dr Aschner.

scholarly journals On the Role of Glial Cells in the Mammalian Nervous System

1974 ◽  
Vol 249 (6) ◽  
pp. 1769-1780
Author(s):  
Bruce K. Schrier ◽  
Edward J. Thompson
Keyword(s):  
Nervous System ◽  
Glial Cells

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.

Glial Cells and Pro-inflammatory Cytokines as Shared Neurobiological Bases for Chronic Pain and Psychiatric Disorders

2020 ◽  
pp. 27-49
Author(s):  
Judith A. Strong ◽  
Sang Won Jeon ◽  
Jun-Ming Zhang ◽  
Yong-Ku Kim
Keyword(s):  
Chronic Pain ◽  
Nervous System ◽  
Psychiatric Disorders ◽  
Inflammatory Cytokines ◽  
Glial Cells ◽  
Neuronal Excitability ◽  
Pro Inflammatory Cytokines

This chapter reviews the roles of cytokines and glial cells in chronic pain and in psychiatric disorders, especially depression. One important role of cytokines is in communicating between activated glia and neurons, at all levels of the nervous system. This process of neuroinflammation plays important roles in pain and depression. Cytokines may also directly regulate neuronal excitability. Many cytokines have been implicated in both pain and psychiatric disorders, including interleukin-1β‎ (IL-1β‎), tumor necrosis factor-α‎, and IL-6. More generally, an imbalance between type 1, pro-inflammatory cytokines and type 2, anti-inflammatory cytokines has been implicated in both pain and psychiatric disorders. Activation of the sympathetic nervous system can contribute to both pain and psychiatric disorders, in part through its actions on inflammation and the cytokine profile.

scholarly journals sli is required for proper morphology and migration of sensory neurons in the Drosophila PNS

2019 ◽  
Vol 14 (1) ◽  
Author(s):  
Madison Gonsior ◽  
Afshan Ismat
Keyword(s):  
Nervous System ◽  
Sensory Neurons ◽  
Glial Cells ◽  
System Development ◽  
Nervous System Development ◽  
Final Position ◽  
Neuron Development ◽  
Guidance Cues ◽  
And Migration

Abstract Neurons and glial cells coordinate with each other in many different aspects of nervous system development. Both types of cells are receiving multiple guidance cues to guide the neurons and glial cells to their proper final position. The lateral chordotonal organs (lch5) of the Drosophila peripheral nervous system (PNS) are composed of five sensory neurons surrounded by four different glial cells, scolopale cells, cap cells, attachment cells and ligament cells. During embryogenesis, the lch5 neurons go through a rotation and ventral migration to reach their final position in the lateral region of the abdomen. We show here that the extracellular ligand sli is required for the proper ventral migration and morphology of the lch5 neurons. We further show that mutations in the Sli receptors Robo and Robo2 also display similar defects as loss of sli, suggesting a role for Slit-Robo signaling in lch5 migration and positioning. Additionally, we demonstrate that the scolopale, cap and attachment cells follow the mis-migrated lch5 neurons in sli mutants, while the ventral stretching of the ligament cells seems to be independent of the lch5 neurons. This study sheds light on the role of Slit-Robo signaling in sensory neuron development.

scholarly journals Neural Control of Immunity in Hypertension: Council on Hypertension Mid Career Award for Research Excellence, 2019

Hypertension ◽  
2020 ◽  
Vol 76 (3) ◽  
pp. 622-628
Author(s):  
Daniela Carnevale
Keyword(s):  
Immune Response ◽  
Nervous System ◽  
Neural Control ◽  
Neural Signals ◽  
The Past ◽  
Target Organs ◽  
Long Time ◽  
The Common ◽  
The Brain

The nervous system and the immune system share the common ability to exert gatekeeper roles at the interfaces between internal and external environment. Although interaction between these 2 evolutionarily highly conserved systems has been recognized for long time, the investigation into the pathophysiological mechanisms underlying their crosstalk has been tackled only in recent decades. Recent work of the past years elucidated how the autonomic nervous system controls the splenic immunity recruited by hypertensive challenges. This review will focus on the neural mechanisms regulating the immune response and the role of this neuroimmune crosstalk in hypertension. In this context, the review highlights the components of the brain-spleen axis with a focus on the neuroimmune interface established in the spleen, where neural signals shape the immune response recruited to target organs of high blood pressure.

The Ferrier Lecture - Neuroglial cells: physiological properties and a potassium mediated effect of neuronal activity on the glial membrane potential

1967 ◽  
Vol 168 (1010) ◽  
pp. 1-21 ◽  
Keyword(s):  
Nervous System ◽  
Glial Cells ◽  
Original Description ◽  
Large Mass ◽  
Electron Microscopic ◽  
Physiological Properties ◽  
Chemical Studies ◽  
Glial Membrane ◽  
Separate Class

Neuroglial cells constitute a separate class of cells in the nervous system; they have been studied intensively since their original description by Virchow in 1846. As a rule anatomists find no difficulty in recognizing them by their staining properties, their shape and configuration as well as by their characteristic location between and around neurons. Electron microscopy has in recent years added much important subcellular detail and has shown how intermingled neurons and glial cells are, being separated from each other by narrow clefts 100 to 200 Å wide (figures 1 A, B and 5, plates 1, 2 and 4). These studies have not changed the well-established grouping of mammalian glial cells into two main classes, the oligodendrocytes and the astrocytes . It is customary to state that glial cells outnumber neurons by 10 to 1 in the vertebrate nervous sytem. They are, however, smaller and according to some rough estimates they make up as much as 50% of the volume of mammalian brains. That glial cells differ significantly from neurons was clear from the beginning because they do not possess axons and, unlike mammalian neurons, they retain their ability to divide throughout life. The possible role of the large mass of glial cells in our nervous system has been of continued interest. During the past decade this interest in the physiology of neuroglia has been reinforced, largely under the stimulus of electron-microscopic and chemical studies of the nervous system. Among the numerous recent reviews and symposia only a few will be mentioned (Windle 1958; Nakai 1963; Mugnaini & Walberg 1964). The recent studies of the physiology of neuroglial cells have been reviewed by Kufller & Nicholls (1966) and a biblio­graphy on neuroglia has been compiled by Little & Morris (1965).

scholarly journals Uncovering Novel Roles of Nonneuronal Cells in Body Weight Homeostasis and Obesity

Endocrinology ◽  
2013 ◽  
Vol 154 (9) ◽  
pp. 3001-3007 ◽  
Author(s):  
Julie A. Chowen ◽  
Jesús Argente ◽  
Tamas L. Horvath
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Glial Cells ◽  
Secondary Complications ◽  
Physiological Regulation ◽  
Structural Support ◽  
The Past ◽  
The Central Nervous System ◽  
Poor Nutrition ◽  
Heterogeneous Class

Glial cells, which constitute more than 50% of the mass of the central nervous system and greatly outnumber neurons, are at the vanguard of neuroendocrine research in metabolic control and obesity. Historically relegated to roles of structural support and protection, diverse functions have been gradually attributed to this heterogeneous class of cells with their protagonism in crescendo in all areas of neuroscience during the past decade. However, this dramatic increase in attention bestowed upon glial cells has also emphasized our vast lack of knowledge concerning many aspects of their physiological functions, let alone their participation in numerous pathologies. This minireview focuses on the recent advances in our understanding of how glial cells participate in the physiological regulation of appetite and systemic metabolism as well as their role in the pathophysiological response to poor nutrition and secondary complications associated with obesity. Moreover, we highlight some of the existing lagoons of knowledge in this increasingly important area of investigation.

scholarly journals Modulation of Neuroinflammation by the Gut Microbiota in Prion and Prion-Like Diseases

Pathogens ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 887
Author(s):  
Josephine Trichka ◽  
Wen-Quan Zou
Keyword(s):  
Nervous System ◽  
Gut Microbiota ◽  
Neurodegenerative Diseases ◽  
Neurodegenerative Disease ◽  
Peripheral Nervous System ◽  
Brain Parenchyma ◽  
Therapeutic Approaches ◽  
Microbial Metabolite ◽  
The Past

The process of neuroinflammation contributes to the pathogenic mechanism of many neurodegenerative diseases. The deleterious attributes of neuroinflammation involve aberrant and uncontrolled activation of glia, which can result in damage to proximal brain parenchyma. Failure to distinguish self from non-self, as well as leukocyte reaction to aggregation and accumulation of proteins in the CNS, are the primary mechanisms by which neuroinflammation is initiated. While processes local to the CNS may instigate neurodegenerative disease, the existence or dysregulation of systemic homeostasis can also serve to improve or worsen CNS pathologies, respectively. One fundamental component of systemic homeostasis is the gut microbiota, which communicates with the CNS via microbial metabolite production, the peripheral nervous system, and regulation of tryptophan metabolism. Over the past 10–15 years, research focused on the microbiota–gut–brain axis has culminated in the discovery that dysbiosis, or an imbalance between commensal and pathogenic gut bacteria, can promote CNS pathologies. Conversely, a properly regulated and well-balanced microbiome supports CNS homeostasis and reduces the incidence and extent of pathogenic neuroinflammation. This review will discuss the role of the gut microbiota in exacerbating or alleviating neuroinflammation in neurodegenerative diseases, and potential microbiota-based therapeutic approaches to reduce pathology in diseased states.

scholarly journals Impaired Mitophagy in Neurons and Glial Cells during Aging and Age-Related Disorders

2021 ◽  
Vol 22 (19) ◽  
pp. 10251
Author(s):  
Vladimir Sukhorukov ◽  
Dmitry Voronkov ◽  
Tatiana Baranich ◽  
Natalia Mudzhiri ◽  
Alina Magnaeva ◽  
...  
Keyword(s):  
Glial Cells ◽  
Brain Aging ◽  
Cellular Level ◽  
Aging Brain ◽  
The Past ◽  
Age Related ◽  
Accumulation Of Damage ◽  
Quantity Control ◽  
The Brain

Aging is associated with a decline in cognitive function, which can partly be explained by the accumulation of damage to the brain cells over time. Neurons and glia undergo morphological and ultrastructure changes during aging. Over the past several years, it has become evident that at the cellular level, various hallmarks of an aging brain are closely related to mitophagy. The importance of mitochondria quality and quantity control through mitophagy is highlighted by the contribution that defects in mitochondria–autophagy crosstalk make to aging and age-related diseases. In this review, we analyze some of the more recent findings regarding the study of brain aging and neurodegeneration in the context of mitophagy. We discuss the data on the dynamics of selective autophagy in neurons and glial cells during aging and in the course of neurodegeneration, focusing on three mechanisms of mitophagy: non-receptor-mediated mitophagy, receptor-mediated mitophagy, and transcellular mitophagy. We review the role of mitophagy in neuronal/glial homeostasis and in the molecular pathogenesis of neurodegenerative disorders, such as Parkinson’s disease, Alzheimer’s disease, and other disorders. Common mechanisms of aging and neurodegeneration that are related to different mitophagy pathways provide a number of promising targets for potential therapeutic agents.

scholarly journals A Review of the Complex Roles of Glial Cells in Alzheimer’s Disease and Potential Glial-Oriented Therapeutic Targets

2018 ◽  
Author(s):  
Saif Shahriar Rahman Nirzhor ◽  
Rubayat Islam Khan ◽  
Sharmind Neelotpol
Keyword(s):  
Quality Of Life ◽  
Central Nervous System ◽  
Nervous System ◽  
Glial Cells ◽  
Therapeutic Targets ◽  
Concentration Of Ions ◽  
The Central Nervous System

The pathogenesis of Alzheimer’s disease (AD) is very complicated and not well-understood. As more and more studies are performed with regards to this disease, new insights are coming to light. Much of the research in AD so far has been very neuron-oriented however, recent studies suggest that certain glial cells i.e. microglia, astrocytes, oligodendrocytes, and NG2 glia are linked to the pathogenesis of AD and may offer several potential therapeutic targets in the long-standing battle against AD. Glial cells are responsible for maintaining homeostasis (i.e. concentration of ions and neurotransmitters) within the neuronal environment of the central nervous system (CNS) and are crucial to the integrity of neurons. This review explores the (1) role of glial cells in AD pathogenesis, (2) complex functionalities of the components involved and (3) potential therapeutic targets that it could eventuate leading to a better quality of life for AD patients.

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