scholarly journals Regulation of solute and water balance and cell volume in the central nervous system.

1992 ◽  
Vol 3 (1) ◽  
pp. 12-27
Author(s):  
K Strange
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Glial Cells ◽  
Molecular Mechanisms ◽  
Mammalian Brain ◽  
Ionic Balance ◽  
Total Brain Volume ◽  
Disease States ◽  
The Central Nervous System ◽  
Physiological Problem

The mammalian brain is composed of four distinct fluid compartments: blood, cerebral spinal fluid, interstitial fluid surrounding glial cells and neurons, and intracellular fluid. Maintenance of the ionic and osmotic composition and volume of these fluids is crucial for the normal functioning of the brain. Small changes in intracellular or extracellular solute composition can dramatically alter neuronal signaling and information processing. Because of the rigid confines of the skull and complex brain architecture, changes in total brain volume can cause devastating neurological damage. As a result, it is not surprising to find that the composition and volume of brain intracellular and extracellular fluids are controlled tightly under both normal conditions and in various disease states. Osmotic and ionic balance in the central nervous system is regulated by solute and water transport across the blood-brain barrier, the choroid plexus, and the plasma membrane of glial cells and neurons. Despite its clinical and physiological significance, however, little is known about the underlying cellular and molecular mechanisms by which the central nervous system's osmotic and ionic balance is maintained. In this review, the current understanding of osmoregulation in the mammalian brain and its role in various disease processes such as hyponatremia, renal failure, and hypernatremia will be summarized. A detailed understanding of brain osmoregulatory processes represents a fundamental physiological problem and is required for the treatment of numerous disease states, particularly those encountered in the practice of nephrology.

scholarly journals Molecular Effects of FDA-Approved Multiple Sclerosis Drugs on Glial Cells and Neurons of the Central Nervous System

2020 ◽  
Vol 21 (12) ◽  
pp. 4229 ◽  
Author(s):  
Kim M. A. De Kleijn ◽  
Gerard J. M. Martens
Keyword(s):  
Multiple Sclerosis ◽  
Central Nervous System ◽  
Nervous System ◽  
Glial Cells ◽  
Molecular Mechanisms ◽  
Dimethyl Fumarate ◽  
Cell Types ◽  
The Central Nervous System ◽  
Molecular Effects ◽  
Approved Drugs

Multiple sclerosis (MS) is characterized by peripheral and central inflammatory features, as well as demyelination and neurodegeneration. The available Food and Drug Administration (FDA)-approved drugs for MS have been designed to suppress the peripheral immune system. In addition, however, the effects of these drugs may be partially attributed to their influence on glial cells and neurons of the central nervous system (CNS). We here describe the molecular effects of the traditional and more recent FDA-approved MS drugs Fingolimod, Dimethyl Fumarate, Glatiramer Acetate, Interferon-β, Teriflunomide, Laquinimod, Natalizumab, Alemtuzumab and Ocrelizumab on microglia, astrocytes, neurons and oligodendrocytes. Furthermore, we point to a possible common molecular effect of these drugs, namely a key role for NFκB signaling, causing a switch from pro-inflammatory microglia and astrocytes to anti-inflammatory phenotypes of these CNS cell types that recently emerged as central players in MS pathogenesis. This notion argues for the need to further explore the molecular mechanisms underlying MS drug action.

Inflammatory cytokines within the central nervous system: sources, function, and mechanism of action

1992 ◽  
Vol 263 (1) ◽  
pp. C1-C16 ◽  
Author(s):  
E. N. Benveniste
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Glial Cells ◽  
Mononuclear Cells ◽  
Neurological Diseases ◽  
Lymphoid Cells ◽  
Disease States ◽  
Activated T Lymphocytes ◽  
The Central Nervous System ◽  
And Function

In recent years, there has been increasing evidence that soluble mediators such as cytokines from activated T lymphocytes and macrophages are able to modulate the growth and function of cells found within the central nervous system (CNS), specifically macroglia and microglia cells. Furthermore, glial cells, upon activation, can secrete immunoregulatory factors that influence lymphoid/mononuclear cells as well as the glial cells themselves. Thus the potential exists for bidirectional communication between lymphoid cells and glial cells within the CNS, which in part is mediated via cytokines. This review describes various neurological disease states in which both immune and glial cells may contribute to inflammation and immunologic events occurring in the CNS. The mechanisms by which glial cells both respond to and synthesize a variety of cytokines within the CNS and the capacity of glial cells to acquire major histocompatibility complex antigens and function as antigen-presenting cells within the CNS are described in detail. The implications of these functions, cytokine secretion and antigen presentation, by glial cells are discussed with respect to neurological diseases associated with autoimmunity and/or inflammation.

Neural Stem Cells to Glial Cells an Important Factor for Brain Injury

2020 ◽  
Author(s):  
Prithiv K R Kumar
Keyword(s):  
Stem Cells ◽  
Central Nervous System ◽  
Nervous System ◽  
Neural Stem Cells ◽  
Glial Cells ◽  
Brain Injuries ◽  
The Body ◽  
The Central Nervous System ◽  
Near Future

Stem cells have the capacity to differentiate into any type of cell or organ. Stems cell originate from any part of the body, including the brain. Brain cells or rather neural stem cells have the capacitive advantage of differentiating into the central nervous system leading to the formation of neurons and glial cells. Neural stem cells should have a source by editing DNA, or by mixings chemical enzymes of iPSCs. By this method, a limitless number of neuron stem cells can be obtained. Increase in supply of NSCs help in repairing glial cells which in-turn heal the central nervous system. Generally, brain injuries cause motor and sensory deficits leading to stroke. With all trials from novel therapeutic methods to enhanced rehabilitation time, the economy and quality of life is suppressed. Only PSCs have proven effective for grafting cells into NSCs. Neurons derived from stem cells is the only challenge that limits in-vitro usage in the near future.

scholarly journals Elucidating the Neuropathologic Mechanisms of SARS-CoV-2 Infection

2021 ◽  
Vol 12 ◽  
Author(s):  
Mar Pacheco-Herrero ◽  
Luis O. Soto-Rojas ◽  
Charles R. Harrington ◽  
Yazmin M. Flores-Martinez ◽  
Marcos M. Villegas-Rojas ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Molecular Mechanisms ◽  
Cell Types ◽  
Public Health Emergency ◽  
Converting Enzyme ◽  
Neurological Manifestations ◽  
Brain Areas ◽  
Angiotensin Converting Enzyme 2 ◽  
The Central Nervous System

The current pandemic caused by the new severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has become a public health emergency. To date, March 1, 2021, coronavirus disease 2019 (COVID-19) has caused about 114 million accumulated cases and 2.53 million deaths worldwide. Previous pieces of evidence suggest that SARS-CoV-2 may affect the central nervous system (CNS) and cause neurological symptoms in COVID-19 patients. It is also known that angiotensin-converting enzyme-2 (ACE2), the primary receptor for SARS-CoV-2 infection, is expressed in different brain areas and cell types. Thus, it is hypothesized that infection by this virus could generate or exacerbate neuropathological alterations. However, the molecular mechanisms that link COVID-19 disease and nerve damage are unclear. In this review, we describe the routes of SARS-CoV-2 invasion into the central nervous system. We also analyze the neuropathologic mechanisms underlying this viral infection, and their potential relationship with the neurological manifestations described in patients with COVID-19, and the appearance or exacerbation of some neurodegenerative diseases.

scholarly journals QT Dispersion: A Predictor of Outcome Following Acute Neurologic Events

Stroke ◽  
2001 ◽  
Vol 32 (suppl_1) ◽  
pp. 343-343
Author(s):  
Elzbieta J Wirkowski ◽  
Joseph Moonjely ◽  
Todd J Cohen ◽  
Stephanie M Manzella ◽  
Richard H Smith ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Functional Outcome ◽  
Qt Dispersion ◽  
Neurological Injury ◽  
Disease States ◽  
Qt Intervals ◽  
The Central Nervous System ◽  
The Difference ◽  
Adjusted Logistic Regression

P26 BACKGROUND: QT dispersion (QTD) reflects heterogeneity of myocardial repolarization, which is modulated by the central nervous system. Pervious studies have shown increased QTD to be a predictor of adverse outcome in various cardiac disease states. However, the central nervous system effects on QTD and its relation to functional outcomes have not been previously studied in patients with acute neurological events (NE). The objective of this study was to determine whether increased QTD is related to functional outcome in patients with cerebrovascular accidents (CVA) and transient ischemic attacks (TIA). METHODS: We studied 140 consecutive pts. aged 72±10 yrs. (48% male) admitted to our institution with NE from 1/98 to 4/98. QTD was calculated from admission EKG as the difference between maximum and minimum QT intervals. 120 pts. had interpretable EKGs with measurable QT intervals in at least 11 of 12 leads. Three separate functional scales (NIHSS, Barthel, and Rankin) were obtained on admission and discharge were recorded. RESULTS: QTD was higher in pts. with intracerebral hemorrhage as compared to CVA and TIA (70±15 vs. 53±27 vs. 48±31 msecs. p=0.03). Increased QTD was associated with lower functional outcome on all 3 scales (all p<0.05) and with higher mortality (p=0.02). QTD was higher in pts. with congestive heart failure (80±43 vs. 47±24 msecs. p=0.006) and carotid disease (59±32 vs. 46±27 msecs. p=0.045) as compared to those without. QTD was not associated with atrial fibrillation or coronary disease. All patients with TIA survived. On multivariate analysis, other independent predictors of poorer outcome were QTD (OR 1.35, 95% CI 1.08–1.68) and a trend towards age (OR 1.07, 95% CI 0.99–1.16). On age-adjusted logistic regression, mortality increased by an OR 1.28, 95% (CI 1.02–1.61) for every 10 msec increase in QTD. CONCLUSION: QTD is an independent predictor of functional outcome and mortality following acute neurological events. In this setting, QTD reflects acute neurological injury as well as underlying heart disease. The mechanism of these findings merits further study.

scholarly journals Novel in vitro Experimental Approaches to Study Myelination and Remyelination in the Central Nervous System

2021 ◽  
Vol 15 ◽  
Author(s):  
Davide Marangon ◽  
Nicolò Caporale ◽  
Marta Boccazzi ◽  
Maria P. Abbracchio ◽  
Giuseppe Testa ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Molecular Mechanisms ◽  
Disease Modeling ◽  
Brain Physiology ◽  
Pathological Conditions ◽  
Approaches To Study ◽  
The Central Nervous System ◽  
Experimental Approaches

Myelin is the lipidic insulating structure enwrapping axons and allowing fast saltatory nerve conduction. In the central nervous system, myelin sheath is the result of the complex packaging of multilamellar extensions of oligodendrocyte (OL) membranes. Before reaching myelinating capabilities, OLs undergo a very precise program of differentiation and maturation that starts from OL precursor cells (OPCs). In the last 20 years, the biology of OPCs and their behavior under pathological conditions have been studied through several experimental models. When co-cultured with neurons, OPCs undergo terminal maturation and produce myelin tracts around axons, allowing to investigate myelination in response to exogenous stimuli in a very simple in vitro system. On the other hand, in vivo models more closely reproducing some of the features of human pathophysiology enabled to assess the consequences of demyelination and the molecular mechanisms of remyelination, and they are often used to validate the effect of pharmacological agents. However, they are very complex, and not suitable for large scale drug discovery screening. Recent advances in cell reprogramming, biophysics and bioengineering have allowed impressive improvements in the methodological approaches to study brain physiology and myelination. Rat and mouse OPCs can be replaced by human OPCs obtained by induced pluripotent stem cells (iPSCs) derived from healthy or diseased individuals, thus offering unprecedented possibilities for personalized disease modeling and treatment. OPCs and neural cells can be also artificially assembled, using 3D-printed culture chambers and biomaterial scaffolds, which allow modeling cell-to-cell interactions in a highly controlled manner. Interestingly, scaffold stiffness can be adopted to reproduce the mechanosensory properties assumed by tissues in physiological or pathological conditions. Moreover, the recent development of iPSC-derived 3D brain cultures, called organoids, has made it possible to study key aspects of embryonic brain development, such as neuronal differentiation, maturation and network formation in temporal dynamics that are inaccessible to traditional in vitro cultures. Despite the huge potential of organoids, their application to myelination studies is still in its infancy. In this review, we shall summarize the novel most relevant experimental approaches and their implications for the identification of remyelinating agents for human diseases such as multiple sclerosis.

Some fly sensory organs are gliogenic and require glide/gcm in a precursor that divides symmetrically and produces glial cells

Development ◽  
2000 ◽  
Vol 127 (17) ◽  
pp. 3735-3743 ◽  
Author(s):  
V. Van De Bor ◽  
R. Walther ◽  
A. Giangrande
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Peripheral Nervous System ◽  
Glial Cell ◽  
Glial Cells ◽  
Sensory Organ ◽  
Asymmetric Distribution ◽  
Sensory Organs ◽  
The Central Nervous System ◽  
Glial Precursor

In flies, the choice between neuronal and glial fates depends on the asymmetric division of multipotent precursors, the neuroglioblast of the central nervous system and the IIb precursor of the sensory organ lineage. In the central nervous system, the choice between the two fates requires asymmetric distribution of the glial cell deficient/glial cell missing (glide/gcm) RNA in the neuroglioblast. Preferential accumulation of the transcript in one of the daughter cells results in the activation of the glial fate in that cell, which becomes a glial precursor. Here we show that glide/gcm is necessary to induce glial differentiation in the peripheral nervous system. We also present evidence that glide/gcm RNA is not necessary to induce the fate choice in the peripheral multipotent precursor. Indeed, glide/gcm RNA and protein are first detected in one daughter of IIb but not in IIb itself. Thus, glide/gcm is required in both central and peripheral glial cells, but its regulation is context dependent. Strikingly, we have found that only subsets of sensory organs are gliogenic and express glide/gcm. The ability to produce glial cells depends on fixed, lineage related, cues and not on stochastic decisions. Finally, we show that after glide/gcm expression has ceased, the IIb daughter migrates and divides symmetrically to produce several mature glial cells. Thus, the glide/gcm-expressing cell, also called the fifth cell of the sensory organ, is indeed a glial precursor. This is the first reported case of symmetric division in the sensory organ lineage. These data indicate that the organization of the fly peripheral nervous system is more complex than previously thought.

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