PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “NEUROGLIA”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed2003

Precursors of neurons, neuroglia, and ependymal cells in the CNS: what are they? Where are they from? How do they get where they are going?

Neurons, neuroglia (astrocytes and oligodendrocytes), and ependymal cells are three distinct categories of neural cells in the central nervous system. In the mature brain and spinal cord, the classical histological criteria define these cells by their microscopic structure very well. During development, the precursors for all of these cells reside within the epithelium of the neural plate and its successor, the neural tube. These precursor cells are the undifferentiated, primitive neuroepithelium of the classical literature. As the cerebral vesicles enlarge and their walls thicken, the primitive neuroepithelial cells elongate, maintaining a radial orientation until they migrate. Although many, but not all, of these cells span the extent of the ventricular wall, they are the precursors of neurons, neuroglia, and ependymal cells. Thus, it is useful to retain their classical designation as primitive neuroepithelial cells and to treat them as neural precursor cells. Neural precursor cells are neither neuroglia nor neurons. It is not appropriate to call them radial glial cells anymore than it is to call them radial neuronal cells. The term "radial glia" has long been used to describe the mature, elongated astrocytes, represented by Bergmann cells in the cerebellum and Müller cells in the retina. Inevitably, during development, transitional forms between neural precursor cells and the neurons, neuroglia, and ependymal cells will occur. Such transitional cells are known as neuroblasts, glioblasts, or ependymoblasts, even though they may be postmitotic. Alternative terms are "immature neurons," "immature neuroglia," and "immature ependymal cells." The migration of many neural precursor cells is accomplished by translocation rather than free cellular locomotion. There is both direct and indirect evidence to document the translocation of the nuclear/perikaryal/somal complex through the leading process of primitive neuroepithelial cells. This is conspicuous in the neocortex, where the discrete radial arrangement of pyramidal cells may result from translocation of neuroblasts, while their leading processes still contact the pial surface. Migration by translocation occurs throughout the CNS. GLIA 43:6-18, 2003.

Animals↗
PubMed1999

Experimental spinal cord injury: spatiotemporal characterization of elemental concentrations and water contents in axons and neuroglia.

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 microM) 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.

Animals↗
PubMed1992

Expression of the non-proliferation-specific protein, statin, in grey matter neuroglia of the aging rat brain.

The monoclonal antibody, S-44, identifies statin, a 57 kDa nuclear protein which appears to be expressed exclusively in non-proliferating cells. We previously demonstrated that in the aging rat corpus callosum approximately one third of neuroglia are statin-negative, suggesting the existence of an unexpectedly large cycling glial compartment. In the present study, double-labeling of individual cultured astroglia with [3H]thymidine and the S-44 antibody provided direct evidence for the non-proliferative status of statin-positive cells. The S-44 antibody was used to immuno-localize statin and thereby determine growth fractions for neuroglia in various grey matter regions of 3-, 18-, and 33-month-old rats. The proportion of statin-negative (cycling) cells for the three ages combined ranged from about 24% in the molecular layer of the dentate gyrus to 38% in the molecular layer of the parietal cortex. In most regions surveyed total glial counts and proportions of statin-positive and -negative cells did not vary significantly as a function of advancing age. These results suggest that (i) as in corpus callosum, pools of cycling neuroglia in various grey matter regions are far in excess of those previously predicted by S-phase labeling with [3H]thymidine or BUdR, and (ii) ratios of proliferating-to-quiescent neuroglia are tightly regulated over much of the animal's adult life span. These conserved ratios may be used as markers of normal CNS senescence, and deviations thereof may indicate the presence and extent of intervening neuropathologic processes.

Aging↗
PubMed1977

[Trace changes in the quantity of RNA in neurons and neuroglia of the hypothalamic nuclei of the brain following short-term intermittent exposure to cold].

Adult albino rats were kept for 2 minutes at --20 degrees C, then for 5 minutes at 25 degrees C, this intermittent cooling being repeated 15 times. One hour after the end of the cooling, the RNA quantity per cell was determined by means of visible cytospectrophotometry to find the increase in the cytoplasm of medial preoptic area neurons and in the nuclei of their glial satellite cells as well as in the nuclei of the perineuronal glial cells of mammillary bodies. Two days after the rats had stayed at the room temperature, these RNA changey bodies the RNA content decreased. 3 days later, the RNA content in the whole neuron--neuroglia unit of the preoptic area returned to normal, while in the neurons and neuroglia of mammillary bodies augmented markedly: this augmentation was found as late as 15 days after the cessation of the cooling. 30 days after the end of the cooling, the RNA quantity in the mammillary body neurons returned to normal, whiel in the neuroglia of this hypothalamic nucleus decreased even lower than the normal level. The authors discuss the problem of a so-called "vegetative memory" and of the involvement of hypothalamic neuron--neuroglia units in the metabolism tranformation dealing with a consolidation of this memory.

Adaptation, Physiological↗
PubMedDate not supplied

[Phospholipid distribution and metabolism in the neurons and neuroglia].

Ratio and intensity of metabolism of phospholipid separate fractions were studied in neurons and neuroglia, isolated from brain cortex by differential ultracentrifugation in density gradient of sucrose and Ficoll with the rate of enriching up to 90% and 80%, respectively. Neurons were characterized by the higher ratio of monophosphoinositides and lysophosphatidyl cholines as compared with neuroglia. Content of phosphatide acids and sphingomyelins was higher in neuroglia. The most specific radioactivity was observed in phosphatide acids both in neurons and neuroglia if 2(-14)C-acetate was administered. Neurons were shown to have higher metabolism of the separate fractions of phospholipids.

Animals↗
PubMed1986

Karyometric, cytophotometric and histoenzymatic studies on neuroglia of rats treated with 1-(2-chloroethyl)-3-cyclohexyl-1-nitrosourea (CCNU/lomoustine).

CCNU is a cytostatic drug, a nitrosourea derivative, used--among others--in therapy of tumors of the central nervous system. Even if the drug is regarded safe for central and peripheral nervous systems, a possibility of harmful effects of CCNU on the central nervous system should be examined caused by the affinity of all nitrosourea derivatives to lipids. This has prompted us to study the drug effect on neuroglia cells in corpus callosum and gyrus cinguli. The drug was administered to rats by the intragastric route in four doses--one dose a week. Three doses of 2.5 mg each were followed by one dose of 5 mg. Some brains were isolated for the studies, and paraffin sections were prepared for karyometric as well as cytophotometric studies and for section staining according to Nissl and Klüver-Barrer techniques 8 days after the last dosage. Brains of other experimental rats served for preparing cryostat sections for demonstration of phosphatase and esterase activities. The studies, conducted after CCNU administration, documented a significant decrease in size of oligodendroglia nuclei and an increase in size of astroglia nuclei. DNA content of neuroglia nuclei was markedly decreased. Histoenzymatic changes in experimental animals were not very pronounced and included a slight increase in TPPase and nonspecific esterase activities as well as a decrease in ATPase activity. Despite the changes in neuroglia cells no damage to corpus callosum myelin sheaths was observed.

Adenosine Triphosphatases↗
PubMed1993

Immunoelectron microscopic localization of basic FGF in neuroglias and neurons of the trigeminal mesencephalic and motor nuclei.

Discrepancies between previous light microscopic studies on the localization of basic fibroblast growth factor (bFGF) in neuroglias and neurons of the normal rat brain prompted us to investigate, by electron microscopy, the subcellular localization of bFGF-like immunoreactivity in neuroglias and neurons of the trigeminal motor and mesencephalic nuclei. Immunostaining intensity differed from astrocyte to astrocyte; in astrocytes labeled heavily with bFGF antiserum, the precise subcellular location of immunoreaction deposits was difficult to determine, whereas mildly labeled astrocytes contained reaction products in subcellular regions apart from gliofilaments, mitochondria and Golgi apparatus. A comparison of immunostained sections with negative control ones at the light and electron microscopic levels revealed that astrocyte nuclei occasionally showed bFGF immunoreactivity. Immunoreactive astrocyte processes were also found in close apposition to blood vessels. bFGF was detected mainly in intracellular structures close to free ribosomes and the endoplasmic reticulum of immunoreactive oligodendrocytes and neurons; microglias rarely showed immunostaining. The nuclei of the cells with bFGF contained immunoreaction deposits of varying intensity, mainly in the euchromatin and rarely in the heterochromatin. Occasionally, bFGF of neuroglial origin accumulated in the vicinity of the interface between neurons and neuroglias. The extracellular matrix was not immunoreactive in any of the areas examined. These findings suggest that certain populations of astrocytes and oligodendrocytes as well as neurons in the normal brain contain bFGF-like substances.

Animals↗
PubMed1989

[Biochemical and morphological changes in the neuroglia in experimental herpetic encephalitis].

The complex virological, biochemical and morphological study permitted to obtain various characteristics of mice herpes encephalitis. The reaction of astrocyte glia at different stages of herpes encephalitis was revealed and analyzed in detail. New data on the dynamics of desoxyribonuclease activity changes in neuroglia and the glial complex formation were obtained. It was shown that the increased DNA-ase activity in neuroglia and the astrocyte activation which morphological manifestation was the formation of glial complexes, may be referred to as processes dealing with barrier and elimination neuroglia functions in herpes encephalitis. The results presented allows to suppose that the severity of the development and outcome of herpes encephalitis mainly depends on the astrocyte glia condition, its potential abilities in appearing of barrier and eliminative functions.

Animals↗
PubMed1980

Neuroglia of the developing optic nerve in the course of Wallerian degeneration.

Unilateral enucleation was performed in 8 days rabbits and morphological changes occurring in the degenerating immature optic nerve were evaluated by means of light and electron microscopy and correlated with histoenzymatic changes in the activity of various phosphatases, esterases and oxidoreductases. The results of these experiments have lead to the following conclusions: 1. In contrast to the marked hyperplasia of the astroglia, the cellularity of the neuroglia of the oligodendroglial line suffered a considerable decrease in the course of Wallerian degeneration of the immature optic nerve. 2. Disconnection of axons from their parental perikaryons caused a considerable delay and reduction of differentiation of the immature neuroglia cells into oligodendrocytes. 3. The histoenzymatic pattern of neuroglia in the immature degenerating optic nerve differs from and bears no relation to that of the normally developing nerve. 4. Cells of the oligodendroglia line, when maturing in contact with degenerating axons are incapable of promoting myelinogenesis. 5. The genetic information contained in both the immature and mature oligodendroglia cells is not the sole factor safeguarding the transformation of these cells into myelinating ones.

Age Factors↗
PubMed2000

Hyperthermic induction of the 27-kDa heat shock protein (Hsp27) in neuroglia and neurons of the rat central nervous system.

The 27-kDa heat shock protein (Hsp27) is constitutively expressed in many neurons of the brainstem and spinal cord, is strongly induced in glial cells in response to ischemia, seizures, or spreading depression, and is selectively induced in neurons after axotomy. Here, the expression of Hsp27 was examined in brains of adult rats from 1.5 hours to 6 days after brief hyperthermic stress (core body temperature of 42 degrees C for 15 minutes). Twenty-four hours following hyperthermia, Western blot analysis showed that Hsp27 was elevated in the cerebral cortex, hippocampus, cerebellum, and brainstem. Immunohistochemistry for Hsp27 revealed a time-dependent, but transient, increase in the level of Hsp27 immunoreactivity (Hsp27 IR) in neuroglia and neurons. Hsp27 IR was detected in astrocytes throughout the brain and in Bergmann glia of the cerebellum from 3 hours to 6 days following heat shock. Peak levels were apparent at 24 hours, gradually declining thereafter. In addition, increases in Hsp27 IR were detected in the ependyma and choroid plexus. Hyperthermia induced Hsp27 IR in neurons of the subfornical organ and the area postrema within 3 hours and reached a maximum by 24 hours with a return to control levels 4-6 days after hyperthermia. Specific populations of hypothalamic neurons also showed Hsp27 IR after hyperthermia. These results demonstrate that hyperthermia induces transient expression of Hsp27 in several types of neuroglia and specific populations of neurons. The pattern of induced Hsp27 IR suggests that some of the activated cells are involved in physiological responses related to body fluid homeostasis and temperature regulation.

Animals↗
PubMed1986

[Periventricular fatty metamorphosis in neuroglia--a morphologic substrate in SIDS].

In 7 of 15 cases of sudden infant death syndrome (SIDS), distinct periventricular fatty metamorphosis of the neuroglia could be demonstrated by a histological staining technique. None of the six children (under 1 year of age) used as a control group whose cause of death was not SIDS showed this morphological change. Thin-layer chromatographic analysis of the lipids accumulated in the glial cells in SIDS established a high amount of esterified cholesterol whereas the content of esterified cholesterol in the control group was low. We presume that fatty metamorphosis of the neuroglia represents the morphological substrate of a metabolic disorder of the sensitive, immature glia of the periventricular white cerebral matter caused by various kinds of damage.

Cerebral Ventricles↗
PubMed1976

The brain of the horseshoe crab (Limulus polyphemus). I. Neuroglia.

The brain of the horseshoe crab, Limulus polyphemus, harbors three populations of neuroglial cells, whose distribution and cellular details are best appreciated by a combination of silver impregnation, scanning, and transmission electron microscopy. Stellate astrocytes envelop neurons as satellite cells, permeate the neuropile, and secrete a framework of sustentacular trabeculae throughout the brain. Velate astrocytes are restricted to Kenyon cells, i.e. small association neurons, of which they harbor up to 150 per neuroglial cell. Vascular neuroglia is composed of glycogen and mitochondria-laden, interlocked cells that form an open meshwork in the hemocoelic spaces of the brain. Aside from supportive functions of neuroglia, the vascular neuroglial cells in particular seem to subserve the role of a metabolic reserve cell for the central nervous system.

Animals↗