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):  
Author(s):  
Judith A. Strong ◽  
Sang Won Jeon ◽  
Jun-Ming Zhang ◽  
Yong-Ku Kim

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.


2019 ◽  
Vol 14 (1) ◽  
Author(s):  
Madison Gonsior ◽  
Afshan Ismat

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.


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).


Author(s):  
Saif Shahriar Rahman Nirzhor ◽  
Rubayat Islam Khan ◽  
Sharmind Neelotpol

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.


PEDIATRICS ◽  
1994 ◽  
Vol 93 (1) ◽  
pp. 156-156
Author(s):  
Thor Willy Ruud Hansen

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.


Development ◽  
1995 ◽  
Vol 121 (2) ◽  
pp. 429-438 ◽  
Author(s):  
A. Giangrande

Fly glial cells in the wing peripheral nervous system of Drosophila melanogaster originate from underlying epithelial cells. Two findings indicate that gliogenesis is closely associated with neurogenesis. First, it only occurs in regions that also give rise to sensory organs. Second, in mutants that induce the development of ectopic sensory organs glial cells develop at new positions. These findings prompted a genetic analysis to establish whether glial and sensory organ differentiation depend on the same genes. Loss of function mutations of the achaete-scute complex lead to a significant reduction of sensory bristles and glial cells. Genes within the complex affect gliogenesis with different strength and display some functional redundancy. Thus, neurogenesis and gliogenesis share the same genetic pathway. Despite these similarities, however, the mechanism of action of the achaete-scute complex seems to be different in the two processes. Neural precursors express products of the complex, therefore the role of these genes on neurogenesis is direct. However, markers specific to glial cells do not colocalize with products of the achaete-scute complex, showing that the complex affects gliogenesis indirectly. These observations lead to the hypothesis that gliogenesis is induced by the presence of sensory organ cells, either the precursor or its progeny.


Author(s):  
Sujata Basu ◽  
Manisha Singh ◽  
Mansi Verma ◽  
Rachana R.

The glial cells along with cells of hematopoietic origin and microvascular endothelia work together to maintain the normal development and/or functioning of the nervous system. Disruption in functional coordination among these cells interrupts the efficiency of the nervous system, leading to neurodegeneration. Various proteins in the nerve cells maintain the normal signaling mechanism with these cells and throughout the body. Structural/functional disorganization of these proteins causes neurodegenerative disorders. The molecular mechanisms involved in these phenomena are yet to be explored extensively from therapeutic perspectives. Through this chapter, the authors have elaborated on less known protein Bcl-2 associated athanogene 3 (BAG3) involved in neurodegeneration. They have explored BAG3 protein and its role in neurodegeneration, protein homeostasis, its mechanism of action, its uses as a drug target, and its uses as a possible diagnostic marker of neurodegeneration.


The Neuron ◽  
2015 ◽  
pp. 213-238
Author(s):  
Irwin B. Levitan ◽  
Leonard K. Kaczmarek

A multitude of chemicals called neurotransmitters mediate intercellular communication in the nervous system. These include acetylcholine, the catecholamines, serotonin, glutamate, GABA, glycine, and a wide variety of neuropeptides. Although they exhibit great diversity in many of their properties, all are stored in vesicles in nerve terminals and are released to the extracellular space via a process requiring calcium ions. Their actions are terminated by reuptake into the presynaptic terminal or nearby glial cells by specific transporter proteins or by their destruction in the extracellular space. The role of neurotransmitters is to alter the properties—chemical, electrical, or both—of some target cell. With the arrival on the scene of the neuropeptides, it has become evident that signaling in the nervous system occurs through the use of rich and varied forms of chemical currency, and that some neurons use more than one type of currency simultaneously.


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