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Journal articles on the topic 'Neuroglia'

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Author: Grafiati

Published: 4 June 2021

Last updated: 31 July 2024

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1

Salkov, V. N., D. N. Voronkov, and V. S. Sukhorukov. "Quantitative changes in ferritin-containing glia in the structures of the substantia nigra in aging and Parkinson’s disease." CLINICAL AND EXPERIMENTAL MORPHOLOGY 13, no. 2 (2024): 20–25. http://dx.doi.org/10.31088/cem2024.13.2.20-25.

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Introduction. Iron accumulates in the substantia nigra (SN) in aging and Parkinson’s disease (PD). However, there is a distinct lack of information about the changes in the metabolism of ferritin–an iron-binding protein in nigral cells–in aging and PD. The aim of the study was to quantify the changes in the number of H- and L-ferritin glia in the SN structures in aging and PD. Materials and methods. We examined autopsies of PD patients (5 cases), mature and elderly people (6 cases), as well as senile people (5 cases). Immunohistochemistry and light microscopy were used to study the location of H- and L-ferritin chains in the SN structures. The density of H– and L–ferritin-containing neuroglia was determined with computer morphometry. Results. In all cases, ferritin was accumulated predominantly in the reticular part of the SN in unpigmented neurons and neuroglial cells. The density of H– and L–ferritin-containing neuroglia in the SN of PD patients and senile people was significantly higher compared to that in mature and elderly people. The same differences between the groups of PD patients and elderly people were found only for the density of H–ferritin-containing neuroglia. Conclusion. The differences revealed between the age groups in the density of H– and L–ferritin-containing neuroglia characterize their increase with age and correspond to the accumulation of iron in the SN during aging. The differences revealed with the same parameters between patients with PD and mature, elderly, and senile patients characterize the imbalance of iron accumulation and oxidation processes in ferritin-containing glial cells of patients with PD. Keywords: aging, Parkinson’s disease, substantia nigra, immunohistochemistry, morphometric, ferritin, neuroglia

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2

Miller, R. H. "Neuroglia." Neurology 48, no. 2 (February 1, 1997): 560. http://dx.doi.org/10.1212/wnl.48.2.560-a.

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3

Min, Kyung-Whan. "Neuroglia." JAMA: The Journal of the American Medical Association 276, no. 10 (September 11, 1996): 837. http://dx.doi.org/10.1001/jama.1996.03540100081038.

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4

Smolič, Tina, Robert Zorec, and Nina Vardjan. "Pathophysiology of Lipid Droplets in Neuroglia." Antioxidants 11, no. 1 (December 23, 2021): 22. http://dx.doi.org/10.3390/antiox11010022.

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In recent years, increasing evidence regarding the functional importance of lipid droplets (LDs), cytoplasmic storage organelles in the central nervous system (CNS), has emerged. Although not abundantly present in the CNS under normal conditions in adulthood, LDs accumulate in the CNS during development and aging, as well as in some neurologic disorders. LDs are actively involved in cellular lipid turnover and stress response. By regulating the storage of excess fatty acids, cholesterol, and ceramides in addition to their subsequent release in response to cell needs and/or environmental stressors, LDs are involved in energy production, in the synthesis of membranes and signaling molecules, and in the protection of cells against lipotoxicity and free radicals. Accumulation of LDs in the CNS appears predominantly in neuroglia (astrocytes, microglia, oligodendrocytes, ependymal cells), which provide trophic, metabolic, and immune support to neuronal networks. Here we review the most recent findings on the characteristics and functions of LDs in neuroglia, focusing on astrocytes, the key homeostasis-providing cells in the CNS. We discuss the molecular mechanisms affecting LD turnover in neuroglia under stress and how this may protect neural cell function. We also highlight the role (and potential contribution) of neuroglial LDs in aging and in neurologic disorders.

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5

Chvátal, Alexandr, and Alexei Verkhratsky. "An Early History of Neuroglial Research: Personalities." Neuroglia 1, no. 1 (August 16, 2018): 245–81. http://dx.doi.org/10.3390/neuroglia1010016.

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Neuroscience, like most other divisions of natural philosophy, emerged in the Hellenistic world following the first experimental discoveries of the nerves connecting the brain with the body. The first fundamental doctrine on brain function highlighted the role for a specific substance, pneuma, which appeared as a substrate for brain function and, being transported through the hollow nerves, operated the peripheral organs. A paradigm shift occurred in 17th century when brain function was relocated to the grey matter. Beginning from the end of the 18th century, the existence of active and passive portions of the nervous tissue were postulated. The passive part of the nervous tissue has been further conceptualised by Rudolf Virchow, who introduced the notion of neuroglia as a connective tissue of the brain and the spinal cord. During the second half of the 19th century, the cellular architecture of the brain was been extensively studied, which led to an in-depth morphological characterisation of multiple cell types, including a detailed description of the neuroglia. Here, we present the views and discoveries of the main personalities of early neuroglial research.

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6

Verkhratsky, Alexei, and Vladimir Parpura. "Introduction to Neuroglia." Colloquium Series on Neuroglia in Biology and Medicine: From Physiology to Disease 1, no. 1 (February 24, 2014): 1–74. http://dx.doi.org/10.4199/c00102ed1v01y201401ngl001.

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7

Stout, Randy F., and Navin Pokala. "Neuroglia inC. elegans." Colloquium Series on Neuroglia in Biology and Medicine: From Physiology to Disease 5, no. 1 (February 27, 2018): i—56. http://dx.doi.org/10.4199/c00160ed1v01y201712ngl011.

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8

Jellinger, K. A. "Neuroglia, 2nd edn." European Journal of Neurology 18, no. 12 (July 28, 2011): e154-e154. http://dx.doi.org/10.1111/j.1468-1331.2011.03492.x.

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9

Somjen, G. G. "The Neuroglia Mystery." Science 260, no. 5116 (June 25, 1993): 1984–85. http://dx.doi.org/10.1126/science.260.5116.1984.

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10

Heneka, Michael T., José J. Rodríguez, and Alexei Verkhratsky. "Neuroglia in neurodegeneration." Brain Research Reviews 63, no. 1-2 (May 2010): 189–211. http://dx.doi.org/10.1016/j.brainresrev.2009.11.004.

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11

Verkhrasky, Alexei, Oleg A. Krishtal, and Geoffrey Burnstock. "Purinoceptors on Neuroglia." Molecular Neurobiology 39, no. 3 (March 13, 2009): 190–208. http://dx.doi.org/10.1007/s12035-009-8063-2.

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Verkhratsky, Alexei, Oleg A. Krishtal, and Geoffrey Burnstock. "Purinoceptors on Neuroglia." Molecular Neurobiology 39, no. 3 (April 28, 2009): 209. http://dx.doi.org/10.1007/s12035-009-8070-3.

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13

St John, James. "Neuroglia—An Open Access Journal." Neuroglia 2, no. 1 (June 4, 2021): 2–3. http://dx.doi.org/10.3390/neuroglia2010002.

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14

Toledano-Díaz, Adolfo, M. Isabel Álvarez, and Adolfo Toledano. "The relationships between neuroglial alterations and neuronal changes in Alzheimer’s disease, and the related controversies I: Gliopathogenesis and glioprotection." Journal of Central Nervous System Disease 14 (January 2022): 117957352211287. http://dx.doi.org/10.1177/11795735221128703.

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Since Alois Alzheimer described the pathology of Alzheimer’s disease in 1907, an increasing number of studies have attempted to discover its causes and possible ways to treat it. For decades, research has focused on neuronal degeneration and the disruption to the neural circuits that occurs during disease progression, undervaluing in some extent the alterations to glial cells even though these alterations were described in the very first studies of this disease. In recent years, it has been recognized that different families of neuroglia are not merely support cells for neurons but rather key and active elements in the physiology and pathology of the nervous system. Alterations to different types of neuroglia (especially astroglia and microglia but also mature oligodendroglia and oligodendroglial progenitors) have been identified in the initial neuropathological changes that lead to dementia, suggesting that they may represent therapeutic targets to prevent neurodegeneration. In this review, based on our own studies and on the relevant scientific literature, we argue that a careful and in-depth study of glial cells will be fundamental to understanding the origin and progression of Alzheimer’s disease. In addition, we analyze the main issues regarding the neuroprotective and neurotoxic role of neuroglial changes, reactions and/or involutions in both humans with Alzheimer’s disease and in experimental models of this condition.

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Stavchansky, Vasily V., Vadim V. Yuzhakov, Larisa E. Sevan’kaeva, Natalia K. Fomina, Anastasia E. Koretskaya, Alina E. Denisova, Ivan V. Mozgovoy, et al. "Melanocortin Derivatives Induced Vascularization and Neuroglial Proliferation in the Rat Brain under Conditions of Cerebral Ischemia." Current Issues in Molecular Biology 46, no. 3 (March 5, 2024): 2071–92. http://dx.doi.org/10.3390/cimb46030133.

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Stroke remains the second leading cause of death worldwide. The development of new therapeutic agents focused on restoring vascular function and neuroprotection of viable tissues is required. In this study the neuroprotective activity of melanocortin-like ACTH(4–7)PGP and ACTH(6–9)PGP peptides was investigated in rat brain at 24 h after transient middle cerebral artery occlusion (tMCAO). The severity of ischemic damage, changes in the proliferative activity of neuroglial cells and vascularization of rat brain tissue were analyzed. The administration of peptides resulted in a significant increase in the volume density of neurons in the perifocal zone of infarction compared to rats subjected to ischemia and receiving saline. Immunohistochemical analysis of the proliferative activity of neuroglia cells using PCNA antibodies showed a significant increase in the number of proliferating cells in the penumbra and in the intact cerebral cortex of rats receiving peptide treatment. The effect of peptides on vascularization was examined using CD31 antibodies under tMCAO conditions, revealing a significant increase in the volume density of vessels and their sizes in the penumbra after administration of ACTH(4–7)PGP and ACTH(6–9)PGP. These findings confirm the neuroprotective effect of peptides due to the activation of neuroglia proliferation and the enhancement of collateral blood flow.

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16

Kozlov, Vadim A., Leonid N. Voronov, Nadezhda V. Smirnova, Pavel B. Karyshev, Anatasia A. Stepanova, Sergey V. Plyukhin, and Elena Yu Lyalina. "COMPARATIVE ANALYSIS OF NEUROGLIAL RELATIONSHIPS IN SOME FORMS OF NEURODEGENERATIVE DISEASES." Acta medica Eurasica, no. 4 (December 26, 2022): 27–36. http://dx.doi.org/10.47026/2413-4864-2022-4-27-36.

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The aim of the study was to compare the measurable quantitative indicators of neurons and neuroglia in the gyrus precentralis region in relatively healthy individuals who died from nonviolent death and not as an outcome of the disease with similar indicators in those who died as a result of lifetime neurodegenerative diseases. Material and methods. 47 cases of nonviolent death were examined: 6 persons were relatively healthy individuals without a history of neurological diseases (average age – 67.0±7.7 years), in 2 persons– parkinsonism was diagnosed in vivo (G20.X, average age 77.0±7.1 years), in 23 persons – G93.4 (unspecified encephalopathy, 51.6±14.1 years), in 13 persons – G31.2 (degeneration of the nervous system caused by alcohol, 55.5±8.4 years). There were 32 men and 15 women. Sex differences were not taken into account in statistical processing. Results. in relatively healthy patients, the median number of neurons (N) is 26.0 (percentiles 10¸90 – 22,0¸29,0 ), coefficient of variation (CV) – 11.0, area of neurons, microns 2 (SN) – 265.3 (234.2¸352.5), CV = 16.6; neuroglia (NG) – 80.0 (75 ¸88), CV = 6.0; neuroglial index (NGI) – 3.1 (2.6¸3.8), CV = 3.2, neuroglial area, microns2 (SNG) – 15.3 (9.9¸25.9, KV = 38.2. In the deceased G20.X – N = 2.0 (1.0¸5.0), p = 0.0116, CV = 54.0, SN = 88.8 (53.6¸117.6), p = 0.0124, CV = 31.1; NG = 32.0 (21.0¸37.0), p = 0.4179, CV = 21.0, SNG = 12.3 (8.1¸20.0), p = 0.0006, CV = 36.1; NGI = 12.2 (6.8¸28.0), p = 0.000, CV = 57.0. In G93.4 – N = 3.0 (1.0¸4.0), p = 0.0065, CV = 35.0, SN = 177.6 (47.9¸299.6), p = 0.0007, CV = 52.4; NG = 83.0 (68.0¸94.0), p = 0.1618, CV = 10, SNG = 14.6 (9.9¸21.0), p = 0.0007, CV = 31.6; NGI = 28.7 (19.3¸83.0), p = 0.0000, CV = 56.0. In G31.2 – N = 15.0 (11.0¸20.0), p = 0.6767, CV = 21.0, SN = 59.7 (37.9¸77.8), p = 0.0000, CV = 28.1; NG = 62.0 (49.0¸77.0), p = 0.0477, CV = 16.0, SNG = 14.6 (9.2¸21.7), p = 0.0122, CV = 33.4; NGI = 3.8 (2.7¸7.0), p = 0.0003, CV = 38.2. Conclusions: 1) in parkinsonism, a significant decrease in the number and area of neurons and neuroglia was revealed; 2) in G93.4, neurons are more involved in the pathological process than glial cells; 3) in G31.2, there is an equally large decrease in the number of neurons and glial cells, but the area of neurons decreases more significantly than in glial cells.

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17

Butt, Arthur, and Alexei Verkhratsky. "Neuroglia: Realising their true potential." Brain and Neuroscience Advances 2 (January 2018): 239821281881749. http://dx.doi.org/10.1177/2398212818817495.

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The name neuroglia is generally translated as nerve glue. In the recent past, this has been used to describe passive structural cells. Presently, this view has been challenged and the true dynamic and multifunctional nature of neuroglia is beginning to be appreciated. In the central nervous system, the main kinds of neuroglia are astrocytes (the primary homeostatic cells that ensure synaptic transmission), oligodendrocytes (which form the myelin that ensures rapid electrical transmission) and microglia (the main immune cells). In the peripheral nervous system, neuroglia comprise Schwann cells, satellite glia and enteric glia. These functionally diverse and specialised cells are fundamental to function at the molecular, cellular, tissue and system levels. Without nerve glue, the body cannot function and the future will begin to unlock their importance in higher cognitive functions that set humans apart from other animals and their true potential as therapeutic targets in neurodegenerative and other diseases.

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18

Maysinger, Dusica, and Jeff Ji. "Nanostructured Modulators of Neuroglia." Current Pharmaceutical Design 25, no. 37 (December 17, 2019): 3905–16. http://dx.doi.org/10.2174/1381612825666190912163339.

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Biological and synthetic nanostructures can influence both glia and neurons in the central nervous system. Neurons represent only a small proportion (about 10%) of cells in the brain, whereas glial cells are the most abundant cell type. Non-targeted nanomedicines are mainly internalized by glia, in particular microglia, and to a lesser extent by astrocytes. Internalized nanomedicines by glia indirectly modify the functional status of neurons. The mechanisms of biochemical, morphological and functional changes of neural cells exposed to nanomedicines are still not well-understood. This minireview provides a cross-section of morphological and biochemical changes in glial cells and neurons exposed to different classes of hard and soft nanostructures.

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19

Kettenmann, H., and A. Verkhratsky. "Neuroglia, der lebende Nervenkitt." Fortschritte der Neurologie · Psychiatrie 79, no. 10 (October 2011): 588–97. http://dx.doi.org/10.1055/s-0031-1281704.

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20

YOUNG, J. Z. "The Concept of Neuroglia." Annals of the New York Academy of Sciences 633, no. 1 Glial-Neurona (December 1991): 1–18. http://dx.doi.org/10.1111/j.1749-6632.1991.tb15590.x.

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21

Verkhratsky, Alexei, Yuri Pankratov, Ulyana Lalo, and Maiken Nedergaard. "P2X receptors in neuroglia." Wiley Interdisciplinary Reviews: Membrane Transport and Signaling 1, no. 2 (January 11, 2012): 151–61. http://dx.doi.org/10.1002/wmts.12.

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22

Kusumarini, Shelly, Lita Rakhma Yustinasari, Eka Pramystha Hestianah, Suryo Kuncorojati, and Tutik Juniastuti. "Mozart KV 448 Menurunkan Densitas dan Aktivitas Neuroglia Hipokampus Mencit (Mus musculus) Selama Stres Prenatal No. 416-KE." Jurnal Sain Veteriner 35, no. 1 (October 24, 2017): 1. http://dx.doi.org/10.22146/jsv.29279.

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The aim of this research was to explore the influence of Mozart KV 448 classical music therapy to the neuroglia cells of mice’s hippocampus that were exposed to stress during prenatal. This research were employing twenty female mices and twenty male mices. Female mices were estrus synchronized with PMSG and hCG then monomating to the males. Pregnant females were then divided into four groups (P0, P1, P2, P3). P0 was as control, P1 was treated by one minute forced swim test, P2 was treated by one minute forced swim test followed by thirtyminutes classical music Mozart KV 448 and P3 was treated by one minute forced swim test followed by sixty minutes classical music Mozart KV 448. This research was carried out for twenty-one days during gestation period. The neuroglia density result was analyzed using ANOVA and Duncan test. The neuroglia activity result wasanalyzed using Kruskal wallis test and Z test. The histology reading showed degradation of density and activity of hippocampus neuroglia.

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Kuzenko, Olena, Yuri Demin, and Yevhen Kuzenko. "RESEARCH OF REPARATIVE MECHANISMS IN THE OPTIC NERVE IN TOXIC NEUROPATHY CAUSED BY Cr (VI)." ScienceRise, no. 6 (December 30, 2020): 31–39. http://dx.doi.org/10.21303/2313-8416.2020.001549.

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Intoxication lesions of the optic nerve (toxic optic neuropathy, TON) most often occur under the influence of exogenous factors, including heavy metals. Сell survival under stress have involves heat shock proteins (HSPs). The aim of the research. To assess the optic nerve’s immunoreactivity to heat shock proteins of the HSP70 and HSP90α families and reveal its relationship with the severity of morphological changes in toxic optic neuropathy caused by Cr (VI). Materials and methods. The study was conducted on 48 mature male rats. The experimental groups were given to drink water with Cr(VI) for 20, 40 and 60 days. This type of water is typical for the water basins in the northern districts of the Sumy region. Optic nerves сhanges under the influence of Cr(VI) have investigated by the morphometric method. Neuroglial cells and capillary endothelial cells were assessed by immunohistochemistry by HSP70α and HSP90 expression for intensity and spatial distribution. Results. The data analysis revealed that Cr (VI) has a neurotoxic effect on the optic nerve with the development of edema, which is manifested by the thickening of nerve fibers. The dynamics of HSP70 immunoexpression in the endothelium of the optic nerve capillaries of rats on 20 and 40 experimental days was characterized by stable values and was 1.5 times higher than the control. The maximum number of positively stained cells for the HSP70 marker was detected in endothelial cells of the microvasculature for 60 days – 82.44±12.42 %. HSP70 levels in neuroglia cells of optic nerve have decreased on day 40 (55.66±11.56% p=0.05) and lower than the control (70.44±4.81 %.) group. Optic nerve capillaries was highest immunoactivity on HSP90 in group II endothelial cells – 51.22±14.57% (p=0.05). The activity of HSP90α protein in optic neuroglia cells was characterized by a gradual increase in the duration of the experiment and was higher by 12, 4 % in experimental group III (81.77±21.67 %) compared with control (71.66±4.95 %). Conclusions. Our study provides an insight into the significant difference in the immunoreactivity of heat shock proteins of the HSP70 and HSP90α families in neuroglia and endothelial cells of the optic nerve capillaries under the influence of Cr(VI). The results obtained suggest that Cr (VI) has a neurotoxic effect on the optic nerve with the development of edema, which is manifested by the thickening of nerve fibers. A comparison of the dynamics of the development of the dystrophic process in the optic nerve with the results of the immunohistochemical analysis showed, that an increase in the thickness of nerve fibers is accompanied by an increase in immunoreactive neuroglial cells (HSP90α) and endothelial cells (HSP70).

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Gundersen, Vidar, Jon Storm-Mathisen, and Linda Hildegard Bergersen. "Neuroglial Transmission." Physiological Reviews 95, no. 3 (July 2015): 695–726. http://dx.doi.org/10.1152/physrev.00024.2014.

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Neuroglia, the “glue” that fills the space between neurons in the central nervous system, takes active part in nerve cell signaling. Neuroglial cells, astroglia, oligodendroglia, and microglia, are together about as numerous as neurons in the brain as a whole, and in the cerebral cortex grey matter, but the proportion varies widely among brain regions. Glial volume, however, is less than one-fifth of the tissue volume in grey matter. When stimulated by neurons or other cells, neuroglial cells release gliotransmitters by exocytosis, similar to neurotransmitter release from nerve endings, or by carrier-mediated transport or channel flux through the plasma membrane. Gliotransmitters include the common neurotransmitters glutamate and GABA, the nonstandard amino acid d-serine, the high-energy phosphate ATP, and l-lactate. The latter molecule is a “buffer” between glycolytic and oxidative metabolism as well as a signaling substance recently shown to act on specific lactate receptors in the brain. Complementing neurotransmission at a synapse, neuroglial transmission often implies diffusion of the transmitter over a longer distance and concurs with the concept of volume transmission. Transmission from glia modulates synaptic neurotransmission based on energetic and other local conditions in a volume of tissue surrounding the individual synapse. Neuroglial transmission appears to contribute significantly to brain functions such as memory, as well as to prevalent neuropathologies.

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Skar, Gwenn. "Neuroglia in Infectious Brain Diseases." Colloquium Series on Neuroglia in Biology and Medicine: From Physiology to Disease 2, no. 2 (March 12, 2015): 1–87. http://dx.doi.org/10.4199/c00125ed1v01y201503ngl005.

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Kettenmann, Helmut, and Alexei Verkhratsky. "Neuroglia: the 150 years after." Trends in Neurosciences 31, no. 12 (December 2008): 653–59. http://dx.doi.org/10.1016/j.tins.2008.09.003.

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Verkhratsky, Alexei, José J. Rodríguez, and Vladimir Parpura. "Neuroglia in ageing and disease." Cell and Tissue Research 357, no. 2 (March 21, 2014): 493–503. http://dx.doi.org/10.1007/s00441-014-1814-z.

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Mohanakumar, Kochupurackal P. "Neuroglia in the Aging Brain." Journal of Chemical Neuroanatomy 27, no. 2 (May 2004): 140–41. http://dx.doi.org/10.1016/j.jchemneu.2004.02.001.

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Handayani, Ety Sri, Zainuri Sabta Nugraha, and Prilly i. Raleka Pahlevawati. "Soursop leaf extract increases neuroglia and hepatic degeneration in female rats." Universa Medicina 34, no. 1 (February 26, 2016): 17. http://dx.doi.org/10.18051/univmed.2015.v34.17-24.

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<p>BACKGROUND<br />Soursop leaf contains annonaceous acetogenins and alkaloids. The<br />acetogenins act as inhibitors of mitochondrial complex I, suppress ATP<br />production and cause cell degeneration, whereas the alkaloids act as<br />neurotoxins. Neuronal degeneration will be followed by an increase in<br />neuroglia (gliosis). Hepatic clear cell foci represent the morphology of liver<br />degeneration. The purpose of this study was to evaluate the effect of soursop<br />leaf extract on number of neuroglia brain gliosis and hepatic clear cells in<br />female rats.</p><p>METHODS<br />This study was an experimental study with a post-test only control group<br />design. Ten female Sprague-Dawley strain rats were divided into one control<br />and one treatment group. The control group was gavaged with distilled water,<br />while the treatment group was gavaged with aqueous soursop leaf extract at<br />a dose of 1000 mg/kgBW/day for 90 days. Rat brain tissue samples were<br />taken at day 91 with a transcardial perfusion technique. The number of<br />neuroglia in rat cerebral cortex, hippocampus, substantia nigra, and nucleus<br />accumbens and the number of hepatic clear cells were determined.<br />Independent t-test was used to examine the differences in the numbers of<br />neuroglia and hepatic clear cells between control and treatment groups</p><p>RESULTS<br />The results of independent t-test analysis found a significant difference in<br />the number of neuroglia in the cerebral cortex (p=0.015) and nucleus<br />accumbens of the rats (p=0.030), and significant differences in the number<br />of hepatic clear cells (p=0.029).</p><p>CONCLUSIONS<br />Aqueous soursop leaf extract orally increases neuroglia of the cerebral cortex<br />and nucleus accumbens, and hepatic degeneration in female rats.</p>

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Peña, Robles, Zhang, and Vazquez. "A Milled Microdevice to Advance Glia-Mediated Therapies in the Adult Nervous System." Micromachines 10, no. 8 (July 31, 2019): 513. http://dx.doi.org/10.3390/mi10080513.

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Neurodegenerative disorders affect millions of adults worldwide. Neuroglia have become recent therapeutic targets due to their reparative abilities in the recycling of exogenous neurotoxins and production of endogenous growth factors for proper functioning of the adult nervous system (NS). Since neuroglia respond effectively to stimuli within in vivo environments on the micron scale, adult glial physiology has remarkable synergy with microscale systems. While clinical studies have begun to explore the reparative action of Müller glia (MG) of the visual system and Schwann Cells (ShC) of the peripheral NS after neural insult, few platforms enable the study of intrinsic neuroglia responses to changes in the local microenvironment. This project developed a low-cost, benchtop-friendly microfluidic system called the glia line system, or gLL, to advance the cellular study needed for emerging glial-based therapies. The gLL was fabricated using elastomeric kits coupled with a metal mold milled via conventional computer numerical controlled (CNC) machines. Experiments used the gLL to measure the viability, adhesion, proliferation, and migration of MG and ShC within scales similar to their respective in vivo microenvironments. Results illustrate differences in neuroglia adhesion patterns and chemotactic behavior significant to advances in regenerative medicine using implants and biomaterials, as well as cell transplantation. Data showed highest survival and proliferation of MG and ShC upon laminin and illustrated a four-fold and two-fold increase of MG migration to dosage-dependent signaling from vascular endothelial growth factor (VEGF) and epidermal growth factor (EGF), respectively, as well as a 20-fold increase of ShC migration toward exogenous brain-derived neurotrophic factor (BDNF), compared to media control. The ability to quantify these biological parameters within the gLL offers an effective and reliable alternative to photolithography study neuroglia and their local ranges on the tens to hundreds of microns, using a low-cost and easily fabricated system.

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Bon, E. I., N. E. Maksimovich, and A. V. Malykhina. "NEUROGLIA AND ITS ROLE IN THE PATHOGENESIS OF ISCHEMIC BRAIN DAMAGE. IMMUNOHISTOCHEMICAL MARKERS OF NEUROGLIA." Вестник Смоленской государственной медицинской академии 20, no. 3 (2021): 18–24. http://dx.doi.org/10.37903/vsgma.2021.3.3.

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Chumasov, E. I., N. A. Maistrenko, P. N. Romashchenko, V. B. Samedov, E. S. Petrova, and D. E. Korzhevskii. "Pathological changes of glial cells in the enteric nervous system of the colon with chronic slow-transit constipation." Сибирский научный медицинский журнал 43, no. 6 (January 11, 2024): 191–202. http://dx.doi.org/10.18699/ssmj20230624.

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The origin, development and differentiation of enteric nervous system neuroglia and its involvement in the pathogenesis of gastrointestinal diseases and neurodegenerative diseases have been little studied.Aim of this work is a comparative morphological study of glial cells in the ganglionic plexuses of the enteric nervous system and analysis of neuroglial relationships in chronic slow-transit constipation using immunohistochemical methods.Material and methods. Resection material obtained at the Department of Faculty Surgery, S.P. Fedorov Faculty of Surgery of S.M. Kirov Military Medical Academy during planned surgical operations was used. The objects of the study were fragments of the sigmoid and colon obtained as a result of surgery for chronic slow-transit constipation (five cases, women aged 37–40 years). The study was carried out using immunohistochemical glial markers (GFAP, S100β protein, etc.).Results. Two types of glia were found in the myenteric ganglionic plexus of the large intestine: astrocyte-like and neurolemmocytic. The astrocyte-like type is similar to the neuroglia of the central nervous system, the neurolemmocytic type is similar to the glia of the autonomic nervous system. It has been established that astrocyte-like glia is found only in the Aauerbach ganglionic plexus, while neurolemmocytes are found in all innervated tissues of the intestinal wall. Reactive, dystrophic and degenerative changes in neurocytes, glial elements, agangliogenosis in the Auerbach plexus were found in all cases of chronic slow-transit constipation. Destructive changes in the neuromuscular terminal plexuses, interstitial edema and inflammatory monocytic reaction and leukocyte infiltration in the intestinal mucosa and intestinal submucosa, found in several cases.Conclusions. The results obtained allow classifying chronic slow-transit constipation as a neurodegenerative disease.

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Hayden, Melvin R. "Overview of Neuroglia Activation, Chronic Neuroinflammation, Remodeling, and Impaired Cognition Due to Perivascular Adipose Tissue-Derived Extracellular Vesicle Exosomes in Obesity and Diabetes." Neuroglia 3, no. 4 (October 4, 2022): 112–38. http://dx.doi.org/10.3390/neuroglia3040008.

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Perivascular adipose tissue (PVAT)-derived extracellular vesicles (EVs) with small exosome(s) (PVAT-dEVexos) from the descending aorta are capable of entering capillaries and systemic circulation. These PVAT-dEVexos are delivered to the central nervous system (CNS) in preclinical, obese, insulin and leptin resistant, diabetic, db/db mouse models and humans with T2DM. Once within the CNS, these exosomes are capable of traversing the blood–brain barrier and the blood-cerebrospinal fluid barrier resulting in activation of the neuroglia microglia cell(s) (aMGCs) and the formation of reactive astrocytes (rACs). The chronic peripheral inflammation in the PVAT via crown-like structures consists of activated macrophages and mast cells, which harbor peripheral adipokines, cytokines, and chemokines (pCC) in addition to the EV exosomes. These pCC are transported to the systemic circulation where they may act synergistically with the PVAT-dEVexos to amplify the activation of neuroglia and result in chronic neuroinflammation. Once activated, the MGCs and ACs will contribute to even greater neuroinflammation via central nervous cytokines/chemokines (cnsCC). Activated neuroglia results in an increase of cnsCC and the creation of a vicious cycle of ongoing chronic neuroinflammation and increased redox stress. The increase in reactive oxygen species (ROS) involves the reactive species interactome that not only include reactive oxygen but also reactive nitrogen and sulfur species wherein a vicious cycle of ROS begetting inflammation and inflammation begetting ROS develops. Thus, the CNS perceives peripheral systemic inflammation from the obese PVAT depots as an injury and a response to injury wound healing mechanism develops with activation of neuroglia, cellular remodeling, neurodegeneration, and impaired cognition.

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Tang, Cha-min, Paula M. Orkand, and Richard K. Orkand. "Coupling and uncoupling of amphibian neuroglia." Neuroscience Letters 54, no. 2-3 (March 1985): 237–42. http://dx.doi.org/10.1016/s0304-3940(85)80085-9.

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Pardo, Carlos A., Diana L. Vargas, and Andrew W. Zimmerman. "Immunity, neuroglia and neuroinflammation in autism." International Review of Psychiatry 17, no. 6 (January 2005): 485–95. http://dx.doi.org/10.1080/02646830500381930.

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Verkhratsky, Alexei, and Vladimir Parpura. "Store-operated calcium entry in neuroglia." Neuroscience Bulletin 30, no. 1 (May 15, 2013): 125–33. http://dx.doi.org/10.1007/s12264-013-1343-x.

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Astion, Michael L., and Richard K. Orkand. "Electrogenic Na+/HCO3?cotransport in neuroglia." Glia 1, no. 5 (1988): 355–57. http://dx.doi.org/10.1002/glia.440010508.

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Zeng, Chih-Wei. "Unraveling the Critical Mechanisms and Functions of Neuroglia in Spinal Cord Injuries." Neuroglia 4, no. 3 (July 24, 2023): 188–90. http://dx.doi.org/10.3390/neuroglia4030013.

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LoPachin, Richard M., Christopher L. Gaughan, Ellen J. Lehning, Yoshiro Kaneko, Thomas M. Kelly, and Andrew Blight. "Experimental Spinal Cord Injury: Spatiotemporal Characterization of Elemental Concentrations and Water Contents in Axons and Neuroglia." Journal of Neurophysiology 82, no. 5 (November 1, 1999): 2143–53. http://dx.doi.org/10.1152/jn.1999.82.5.2143.

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To examine the role of axonal ion deregulation in acute spinal cord injury (SCI), white matter strips from guinea pig spinal cord were incubated in vitro and were subjected to graded focal compression injury. At several postinjury times, spinal segments were removed from incubation and rapidly frozen. X-ray microanalysis was used to measure percent water and dry weight elemental concentrations (mmol/kg) of Na, P, Cl, K, Ca, and Mg in selected morphological compartments of myelinated axons and neuroglia from spinal cord cryosections. As an index of axon function, compound action potentials (CAP) were measured before compression and at several times thereafter. Axons and mitochondria in epicenter of severely compressed spinal segments exhibited early (5 min) increases in mean Na and decreases in K and Mg concentrations. These elemental changes were correlated to a significant reduction in CAP amplitude. At later postcompression times (15 and 60 min), elemental changes progressed and were accompanied by alterations in compartmental water content and increases in mean Ca. Swollen axons were evident at all postinjury times and were characterized by marked element and water deregulation. Neuroglia and myelin in severely injured epicenter also exhibited significant disruptions. In shoulder areas (adjacent to epicenter) of severely injured spinal strips, axons and mitochondria exhibited modest increases in mean Na in conjunction with decreases in K, Mg, and water content. Following moderate compression injury to spinal strips, epicenter axons exhibited early (10 min postinjury) element and water deregulation that eventually recovered to near control values (60 min postinjury). Na+ channel blockade by tetrodotoxin (TTX, 1 μM) perfusion initiated 5 min after severe crush diminished both K loss and the accumulation of Na, Cl, and Ca in epicenter axons and neuroglia, whereas in shoulder regions TTX perfusion completely prevented subcellular elemental deregulation. TTX perfusion also reduced Na entry in swollen axons but did not affect K loss or Ca gain. Thus graded compression injury of spinal cord produced subcellular elemental deregulation in axons and neuroglia that correlated with the onset of impaired electrophysiological function and neuropathological alterations. This suggests that the mechanism of acute SCI-induced structural and functional deficits are mediated by disruption of subcellular ion distribution. The ability of TTX to reduce elemental deregulation in compression-injured axons and neuroglia implicates a significant pathophysiological role for Na+ influx in SCI and suggests Na+ channel blockade as a pharmacotherapeutic strategy.

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Mutso, Margit, James A. St John, Zheng Lung Ling, Felicity J. Burt, Yee Suan Poo, Xiang Liu, Eva Žusinaite, et al. "Basic insights into Zika virus infection of neuroglial and brain endothelial cells." Journal of General Virology 101, no. 6 (June 1, 2020): 622–34. http://dx.doi.org/10.1099/jgv.0.001416.

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Zika virus (ZIKV) has recently emerged as an important human pathogen due to the strong evidence that it causes disease of the central nervous system, particularly microcephaly and Guillain–Barré syndrome. The pathogenesis of disease, including mechanisms of neuroinvasion, may include both invasion via the blood–brain barrier and via peripheral (including cranial) nerves. Cellular responses to infection are also poorly understood. This study characterizes the in vitro infection of laboratory-adapted ZIKV African MR766 and two Asian strains of (1) brain endothelial cells (hCMEC/D3 cell line) and (2) olfactory ensheathing cells (OECs) (the neuroglia populating cranial nerve I and the olfactory bulb; both human and mouse OEC lines) in comparison to kidney epithelial cells (Vero cells, in which ZIKV infection is well characterized). Readouts included infection kinetics, intracellular virus localization, viral persistence and cytokine responses. Although not as high as in Vero cells, viral titres exceeded 104 plaque-forming units (p.f.u.) ml−1 in the endothelial/neuroglial cell types, except hOECs. Despite these substantial titres, a relatively small proportion of neuroglial cells were primarily infected. Immunolabelling of infected cells revealed localization of the ZIKV envelope and NS3 proteins in the cytoplasm; NS3 staining overlapped with that of dsRNA replication intermediate and the endoplasmic reticulum (ER). Infected OECs and endothelial cells produced high levels of pro-inflammatory chemokines. Nevertheless, ZIKV was also able to establish persistent infection in hOEC and hCMEC/D3 cells. Taken together, these results provide basic insights into ZIKV infection of endothelial and neuroglial cells and will form the basis for further study of ZIKV disease mechanisms.

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Su, Dan, Xiaofeng Guo, Leyi Huang, Huilin Ye, Zhiguo Li, Longfa Lin, Rufu Chen, and Quanbo Zhou. "Tumor-neuroglia interaction promotes pancreatic cancer metastasis." Theranostics 10, no. 11 (2020): 5029–47. http://dx.doi.org/10.7150/thno.42440.

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Robinson, E. Hampson, M. Munro, and D. Vaney. "Unidirectional coupling of gap junctions between neuroglia." Science 262, no. 5136 (November 12, 1993): 1072–74. http://dx.doi.org/10.1126/science.8093125.

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Ariai, Shafie, Andrei Koerbel, Antje Bornemann, Matthias Morgala, and Marcos Tatagiba. "Cerebellopontine Angle Arachnoid Cyst Harbouring Ectopic Neuroglia." Pediatric Neurosurgery 41, no. 4 (2005): 220–23. http://dx.doi.org/10.1159/000086566.

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Loane, David J., Bogdan A. Stoica, and Alan I. Faden. "Metabotropic glutamate receptor-mediated signaling in neuroglia." Wiley Interdisciplinary Reviews: Membrane Transport and Signaling 1, no. 2 (January 11, 2012): 136–50. http://dx.doi.org/10.1002/wmts.30.

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45

Hajati Pishvari, Mohammad Hossein, Yousef Panahi, and Gholamreza Hamidian. "Effects of Cabergoline and Levetiracetam on the Histological and Stereological Structure of the Cerebral Cortex, Hippocampus and Cerebellum of Rats With Pentylenetetrazol-Induced Seizure." Journal of Guilan University of Medical Sciences 32, no. 1 (April 1, 2023): 18–29. http://dx.doi.org/10.32598/jgums.32.1.1953.3.

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Background: Epilepcy is a chronic neurological disease, and due to its complex mechanism, the current therapeutic drugs for it are not effective enough. It may have a non-neurological origin such as astrocytes and microglia. Objective This study aims to investigate the effect of cabergoline and levetiracetam (alone or combined) on the histological and stereological structure of the cerebral cortex, hippocampus, and cerebellum in rats with pentylenetetrazol (PTZ)-induced seizure. Methods: In this experimental study, samples were 30 female rats in five groups of control, seizure (PTZ-induced kindling), seizure+levetiracetam, seizure+cabergoline, seizure+levetiracetam+cabergoline. Levetiracetam and cabergoline were used at 50 and 0.05 mg/kg doses, respectively, and half of these doses were used in the seizure+levetiracetam+cabergoline group. After anesthesia, animals’ brain tissue was removed and after preparing tissue slices, the number of neurons and neuroglia was examined using stereology technique. Results: In the cerebral cortex and in the molecular and granular layers of the cerebellum, the numbers of neurons and neuroglia in the treatment groups were not significantly different from those in the control group, but a significant decrease was observed in the CA1, CA2, and CA3 regions of the hippocampus in the seizure group compared to the control group. In dentate gyrus, the number of neurons in all treatment groups and the number of neuroglia in the seizure group showed a significant decrease compared to the control group. In the Purkinje layer of the cerebellum, there was no significant change in the number of neurons compared to that in the control group. Conclusion: The hippocampus is more involved in the occurrence of seizure activity than other parts of the brain. Neurons and neuroglia play an essential role in seizures, but more studies are needed for determining the relationship between the number of these cells and the use of cabergoline because their number decreases in different parts of the hippocampus following chronic seizures, where the relationship is different between dendrite gyrus and CA regions.

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Surbakti, Khairul. "Overview of Cellular Aspects of the Nervous System: A Narrative Literature Review." Sriwijaya Journal of Neurology 1, no. 1 (April 26, 2023): 19–25. http://dx.doi.org/10.59345/sjn.v1i1.30.

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The structure of neurons varies so much that each neuron is adapted to perform a specific function. Although their functions may vary slightly, neurons have three common components, namely the cell body (soma), dendrites (thin branching fibers from the cell), and the axon. This literature review aimed to describe the cellular aspect of the system nerves in the human body. The cellular constituents of a typical neuron include microtubules (transporters within the cell), neurofibrils (thin supporting fibers extending throughout the neuron), microfilaments (proteins thought to be involved in the transport of cellular products), and Nissl bodies (endoplasmic reticulum and ribosomes). Involved in protein synthesis. Although most neurons are non-dividing cells, some continue to divide after birth; for example, the olfactory neurons in the nose continue to divide throughout life. In conclusion, there are two basic types of cells comprising nervous tissue: neurons and supporting neuroglia. Neurons are electrically excitable cells and transmit electrical or chemical information between other neurons or to effector organs. Neuroglial cells provide structural support, protection, and nutrition for neurons and facilitate neurotransmission.

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González Rivera, Ivette, Diana Berenice Paz Trejo, Oscar Galicia Castillo, and Hugo Sánchez Castillo. "Implicaciones del sistema serotoninérgico y la neuroglia en lo mecanismos del estrés: Una breve revisión." Psicología Iberoamericana 26, no. 1 (April 17, 2020): 22–30. http://dx.doi.org/10.48102/pi.v26i1.30.

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La respuesta de estrés puede variar dependiendo de la intensidad del estresor, así como de factores inherentes al organismo. De manera general, cuando un sujeto desarrolla trastornos relacionados con el estrés, ocurren cambios anatómicos y fisiológicos en el sistema nervioso central ligados a los síntomas que se presentan. Comúnmente se usan fármacos serotoninérgicos como tratamiento para dichos síntomas; sin embargo, se desconoce la acción precisa de éstos sobre la actividad neural y se conoce mucho menos sobre la participación de la neuroglia en este proceso. El presente artículo muestra la relevancia del sistema serotoninérgico en la respuesta de estrés, así como la posible participación de la neuroglia, particularmente de los astrocitos, como una clave para entender mejor los mecanismos del estrés y la recuperación del sistema por vías serotoninérgicas particulares.

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Arranz, Marcos. "Publisher’s Note: Resumed Publication of Neuroglia by MDPI." Neuroglia 2, no. 1 (April 27, 2021): 1. http://dx.doi.org/10.3390/neuroglia2010001.

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Gawlińska, Kinga, Małgorzata Frankowska, Dawid Gawliński, Marcin Piechota, Michał Korostyński, and Małgorzata Filip. "Cocaine Administration and Its Abstinence Conditions Modulate Neuroglia." International Journal of Molecular Sciences 21, no. 21 (October 27, 2020): 7970. http://dx.doi.org/10.3390/ijms21217970.

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Cocaine induces neuronal changes as well as non-neuronal (astrocytes, microglia, oligodendroglia) mechanisms, but these changes can also be modulated by various types of drug abstinence. Due to the very complex and still incompletely understood nature of cocaine use disorder, understanding of the mechanisms involved in addictive behavior is necessary to further search for effective pharmacotherapy of this disease. The aim of this study was to investigate changes at the gene and protein levels associated with glial cell activity after cocaine exposure, as well as during early cocaine abstinence (3 days) with extinction training or in home cage isolation. Cocaine self-administration significantly decreased myelin regulatory factor (MYRF) and cyclic nucleotide phosphodiesterase (CNP) expression in the hippocampus as well as pleckstrin (PLEK) and T-lymphocyte activation antigen (CD86) in the rat striatum. Depending on cocaine abstinence conditions, microglial PLEK expression was increased through extinction training but did not change in the home cage isolation. In addition, downregulation of gene expression associated with oligodendrocytes (CNP, MYRF) and microglia regulator of G protein signaling 1 (RGS1) was observed in the hippocampus, regardless of the type of drug abstinence, while downregulation of myelin and lymphocyte protein (MAL) expression was found only in rats exposed to abstinence in the home cage. Taken together, the presented results strongly suggest that cocaine abstinence evokes significant changes in gene expression associated with the proper functioning of glial cells, suggesting their significant involvement in adaptive changes in the brain associated with cocaine exposure. Interestingly, drug abstinence conditions are important factors influencing observed changes at the transcript levels of selected genes, which may be of clinical interest.

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Liu, Qianqian, Rui Li, Wei Yang, Ranji Cui, and Bingjin Li. "Role of neuroglia in neuropathic pain and depression." Pharmacological Research 174 (December 2021): 105957. http://dx.doi.org/10.1016/j.phrs.2021.105957.

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