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Results for “Astrocyte morphology”

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PubMed2002

Vascular endothelial growth factor is expressed in multiple sclerosis plaques and can induce inflammatory lesions in experimental allergic encephalomyelitis rats.

The active lesions in multiple sclerosis (MS) are characterized by blood-brain-barrier (BBB) breakdown, upregulation of adhesion molecules on capillary endothelial cells, and perivascular inflammation, suggesting that altered vessel permeability and activated endothelial cells are involved in the pathogenesis of the disease. Vascular endothelial growth factor (VEGF) mediates multiple aspects of blood vessel physiology, including regulation of growth, permeability, and inflammation. To investigate a possible relationship between VEGF expression and CNS autoimmune disease, we examined VEGF expression in MS plaques compared to normal white matter by immunohistochemistry and in situ hybridization. VEGF expression was consistently upregulated in both acute and chronic MS plaques. We also examined VEGF expression during the course of experimental allergic encephalomyelitis (EAE) in rats. VEGF-positive cells with astrocytic morphology increased in the spinal cord during the development of EAE and were found in association with inflammatory cells. Furthermore, intracerebral infusion of VEGF in animals previously immunized with myelin basic protein induced an inflammatory response in the brain, whereas infusion of vehicle, or infusion of VEGF in naive animals, did not. These results suggest that overexpression of VEGF may exacerbate the inflammatory response in autoimmune diseases of the CNS by inducing focal BBB breakdown and migration of inflammatory cells into the lesions.

Animals↗
PubMed1981

Cellular localization and regulation of glutamine synthetase in primary cultures of brain cells from newborn mice.

The cellular distribution of glutamine synthetase was determined by indirect immunofluorescence in cultures of dissociated brain cells from newborn mice. The enzyme could be detected in about 40% of all cells, among which cells with astrocytic morphology were clearly identified. Treatment with the glucocorticoid dexamethasone led to a strong increase in the number of positivity stained cells. Enzyme induction by dexamethasone was maximal after 36 h and at a concentration of 0.1 micrometer. Under these conditions glutamine synthetase specific activity was elevated about six fold. Steroid hormones other than corticosteroids had no effects. The basal activity in these cultures was near that found in brains of newborn mice, but far below the activity in adult brains, showing that in culture the normal development of these cells is disturbed. A comparison of glial and neuronal cell lines showed that glutamine synthetase is present in both types of cell lines at a very low specific activity. Inducibility of this enzyme by dexamethasone was found in glial but not in neuronal cell lines.

Aging↗
PubMed1990

Protease nexin-1. Localization in the human brain suggests a protective role against extravasated serine proteases.

Protease nexin-1 (PN-1) is a potent thrombin inhibitor that is identical to the glia-derived neurite-promoting factor or glia-derived nexin. Here we report immunocytochemical studies of adult human cerebral cortex that revealed the presence of strong immunoreactivity for PN-1 in capillaries and in the smooth muscle cells of arteries and arterioles. Expression of PN-1 was also abundant in astroglial processes in the parenchyma and in perivascular astroglial endfeet of human cerebral cortex. In situ hybridization with an 35S-labeled RNA antisense probe for PN-1 resulted in significant labeling of astrocytes and blood vessels. Because thrombin is known to cause retraction of neurites and modification of astrocytic morphology at low concentrations, PN-1 around blood vessels may play a major protective role against extravasation of thrombin and possibly other serine protease into the human brain.

Alzheimer Disease↗
PubMed1973

Parainfluenza virus Sendai infection in macrophages, ependyma, choroid plexus, vascular endothelium and respiratory tract of mice.

Immunofluorescent observations showed that after intranasal instillation of parainfluenza 1 (Sendai) virus into adult mice, infection is confined to the epithelial lining of the larger airways. Alveolar macrophages were not significantly involved, although they could be infected in vitro. In suckling mice, the infection was more acutely lethal and extended into the terminal air spaces. The intranasal susceptibility of adult mice was not reproducibly affected by treatment with potent antithymocyte serum, and there were no obvious pathogenic effects when heterologous antiserum was instilled intranasally into infected mice. Peritoneal macrophages were infected by intraperitoneally injected Sendai virus, with production of a highly viscous peritoneal exudate. Kupffer cells of the liver and endothelial cells in large veins and auricles were infected by intravenously injected virus. When injected intracerebrally, Sendai virus infected ependyma and choroid plexus epithelium. Adult mice often survived, in spite of ependymal destruction and changes in ventricular morphology. Astrocytes were activated but not infected.

Animals↗
PubMed1996

Adult schizophrenic-like variant of adrenoleukodystrophy.

A 35-year-old man died after 30 months following the onset of the disease. There was a history of changes in his mental condition, including disturbances of behavior as well as the evidence of progressing dementia. The patient revealed gait disturbances and finally became bed ridden. Bizarre behavior and changes of mood with concurrent growing irritability which predominated during the course of disease, may explain the initial diagnosis of schizophrenia. Then cerebellar and spastic movement disorders leading to paraparesis and sphincters disturbances developed. Clinical symptoms of adrenal failure were not found apart from episodes of arterial pressure fall. After two years a magnetic resonance imaging (MRI) revealed an extensive diffuse demyelinative process in white matter of cerebral and cerebellar hemispheres. Activity of lysosomal enzymes was normal. A general autopsy revealed atrophy of adrenal cortex and the presence of ballooned cells with striated cytoplasm in the reticular and fasciculate zones. Neuropathological examination revealed an extensive demyelination of white matter in cerebral and cerebellar hemispheres and of the long paths of the brain stem, corresponding to changes in MRI examination. Within demyelination areas damage of axons and diffuse cellular and fibrous gliosis were found as well as perivascular lymphocytic infiltrations with the presence of strong PAS (+) and Sudan (+) macrophages. Immunocytochemical reactions with HAM-56 and RCA1 in macrophages were positive. Electron microscopy examination revealed lamellar inclusions in cytoplasm of macrophages. Similar structures were present in the lysosomes of astrocytes. Morphological examination of adrenal glands as well as morphological and ultrastructural study of the brain allowed us to diagnose the cerebral form of adrenoleukodystrophy (ALD). Topography and character of the brain changes seems to be in keeping with a rare schizophrenic-like variant of ALD with progressive dementia. Abnormal plasma profile and increased VLCFA concentration in the patient's 13-year-old daughter confirm the ALD diagnosis.

Adrenoleukodystrophy↗
PubMed1997

A common morphological response of astrocytes to various injuries: "dark" astrocytes. A light and electron microscopic analysis.

Our previous studies showed that neurons became argyrophilic following different kinds of brain injuries. In the present study we demonstrated that astrocytes could also become argyrophilic following compressive or concussive head injuries and following intraperitoneal administration of pentylenetetrazole or kainic acid. Furthermore the soma, nucleus and processes of these argyrophilic astrocytes were shown in other preparations to be hyper-basophilic with the light microscope, and hyper-electron dense and shrunken at the ultrastructural level. When the head injuries were inflicted either at the 15th min. of perfusion-fixation or at the 30th min. of transcardial perfusion with chilled physiological saline, several astrocytes also became argyrophilic, hyper-basophilic, shrunken and hyper-electron dense. These data indicate that (i) the intracellular pathological event in these astrocytes is similar to that of "dark" neurons or "dark" cells of non-neural tissues, (ii) the formation of "dark" astrocytes can be independent of the actual state of metabolism, and (iii) the "dark" morphological state of astrocytes might have a role in neuropathological processes.

Animals↗
PubMed1991

Adrenalin activation of beta 2-adrenoceptors stimulates morphological changes in astrocytes (pituicytes) cultured from adult rat neurohypophyses.

Neurohypophysial astrocytes, the pituicytes, are known to undergo morphological changes in vivo in response to stimuli that increase the demand for hormone secretion. Similar changes have been induced by beta-adrenergic stimulation both in the isolated, but otherwise intact, neural lobe and in pituicytes cultured from adult rats. Since the predominant beta-receptor subtype in the neural lobe is beta 2, we investigated the possibility that beta 2-receptor activation is mainly responsible for the observed pituicyte responses. In one experiment, cultured pituicytes were induced by noradrenalin to change from flattened amorphous to stellate morphology. Addition of the beta 2-antagonist IPS 339, but not the beta 1-antagonist practolol, significantly reduced (by 30-60%) the number of cells transformed by noradrenalin. In a second experiment, adrenalin, by definition a more potent beta 2-agonist, transformed significantly more pituicytes into stellate shapes than did noradrenalin at the same concentrations (100% vs. 60% increase, respectively). These results support the idea that beta 2-adrenergic receptors are involved in neurohypophysial plasticity. Also, since the neural lobe is outside of the bloodbrain barrier, these findings suggest that adrenal catecholamines participate in altering pituicyte morphology.

Adrenergic beta-Agonists↗
PubMed2004

Aggregation of integrins and RhoA activation are required for Thy-1-induced morphological changes in astrocytes.

Thy-1, a cell adhesion molecule abundantly expressed in mammalian neurons, binds to a beta(3)-containing integrin on astrocytes and thereby stimulates the assembly of focal adhesions and stress fibers. Such events lead to morphological changes in astrocytes that resemble those occurring upon injury in the brain. Extracellular matrix proteins, typical integrin ligands, bind to integrins and promote receptor clustering as well as signal transduction events that involve small G proteins and cytoskeletal changes. Here we investigated the possibility that the cell surface protein Thy-1, when interacting with a beta(3)-containing integrin on astrocytes, could trigger signaling events similar to those generated by extracellular matrix proteins. DI-TNC(1) astrocytes were stimulated with Thy-1-Fc immobilized on beads, and increased RhoA activity was confirmed using an affinity precipitation assay. The effect of various inhibitors on the cellular response was also studied. The presence of Y-27632, an inhibitor of Rho kinase (p160ROCK), a key downstream effector of RhoA, significantly reduced focal adhesion and stress fiber formation induced by Thy-1. Similar effects were obtained when astrocytes were treated with C3 transferase, an inhibitor of RhoA. Alternatively, astrocytes were transfected with an expression vector encoding fusion proteins of enhanced green fluorescent protein with either the Rho-binding domain of Rhotekin, which blocks RhoA function, or the dominant-negative N19RhoA mutant. In both cases, Thy-1-induced focal adhesion formation was inhibited. Furthermore, we observed that RhoA activity after stimulation with soluble Thy-1-Fc molecule was augmented upon further cross-linking using protein A-Sepharose beads. The same was shown by cross-linking beta(3)-containing integrin with anti-beta(3) antibodies. Together, these results indicate that Thy-1-mediated astrocyte stimulation depended on beta(3) integrin clustering and the resulting increase in RhoA activity.

Amides↗
PubMed2004

Delayed but sustained induction of mitogen-activated protein kinase activity is associated with beta-adrenergic receptor-mediated morphological differentiation of astrocytes.

Astroglial beta-adrenergic receptors (beta-ARs) are functionally linked to regulate cellular morphology. In primary cultures, the beta-AR agonist isoproterenol (ISP) can transform flat polygonal astrocytes into process-bearing, mature stellate cells by 48 h, an effect that can be blocked by the beta-AR antagonist, propranolol. ISP induced immediate activation of protein kinase A (PKA) which persisted up to 2 h, with no visible change in cell morphology. However, activation of PKA was sufficient to drive the process of transformation to completion, suggesting the involvement of downstream regulators of PKA. In addition to PKA inhibitors, the mitogen-activated protein kinase (MAPK) kinase inhibitor PD098059 also blocked ISP-induced morphological transformation. ISP treatment resulted in a biphasic response of cellular phosphorylated MAPK (phosphorylated extracellular signal-regulated kinase; p-ERK) level: an initial decline in p-ERK level followed by a sustained induction at 12-24 h, both of which were blocked by PKA inhibitor. The induction in pERK level coincided with initiation of morphological differentiation of the astrocytes and nuclear translocation of p-ERK. A long-lasting activation of p-ERK activity by ISP, at a later stage, appears to be critical for the transformation of astrocytes.

Adrenergic beta-Agonists↗
PubMed1981

Morphological analysis of astrocytes in the bullfrog (Rana catesbeiana) spinal cord with special reference to the site of attachment of their processes.

An attempt was made to elucidate the morphological features of astrocytes in the bullfrog spinal cord by means of a combination of electron microscopy, the Golgi method, and the intravascular dye injection method. Astrocytic somata are densely concentrated both in the wall of the central canal and in its proximity, and diffusely distributed in the intermediate and the ventral part of the gray matter. The most complicated and densest vascular network is found in the dorsal part of the gray matter. There is little correlation between the density of the distribution of astrocytic somata and that of the vascular network. Each astrocyte emits one process and ramifies by repeated bifurcations as it approaches the white matter or enters it. All these branching processes reach the pial surface of the spinal cord (the principal processes). Total rostrocaudal extent of their ramification is within 400 micron. A great number of small lateral offshoots (the secondary processes) arise both from the somata and the principal processes. Electron microscopy of vessel walls and the pial surface revealed that the principal processes attach to the subpial basement membrane with a specialized structure, an electron-dense layer, while the secondary processes merely surround blood vessels in a mode of juxtaposition. Comparison between amphibian and mammalian astrocytes is made regarding the site of attachment of their processes.

Animals↗
PubMed2003

Subpopulation of nestin-expressing progenitor cells in the adult murine hippocampus shows electrophysiological and morphological characteristics of astrocytes.

Based on the expression of glial fibrillary acidic protein (GFAP), a recent hypothesis considered stem or progenitor cells in the adult hippocampus to be a type of astrocyte. In a complementary approach, we used transgenic mice expressing green fluorescent protein (GFP) under the promoter for nestin, an intermediate filament present in progenitor cells, to demonstrate astrocytic features in nestin-GFP-positive cells. Morphologically, two subpopulations of nestin-GFP-positive cells were distinguishable; one had an elaborate tree of processes in the granule cell layer and expression of GFAP (but not of S100beta, another astrocytic marker). Electron microscopy revealed vascular end feet of nestin-positive cells, further supporting astrocytic differentiation. Electrophysiological examination of nestin-GFP-positive cells on acutely isolated hippocampal slices showed passive current characteristics of astrocytes in one subset of cells. Among the nestin-GFP-expressing cells with lacking astrocytic features, two cell types could be identified electrophysiologically: cells with delayed-rectifying potassium currents and a very small number of cells with sodium currents, potentially representing signs of the earliest steps of neuronal differentiation.

Age Factors↗
PubMed1989

[Morphology of glial cells in the lower olivary complex of the pigeon (Columba livia). I. Astrocytes].

The morphologic peculiarities of astrocytes in the lower olivary complex (LOC of a pigeon were examined at light and electron microscopic level. Usage of histological technique established the presence of three varieties: fibrous, real protoplasmic and covered type of astrocytes. In LOC of a pigeon most of astrocytes, observed by the electron microscope, possessed in their cytoplasm bunches of filaments, which passed and proceeded along side to astrocytic arborizations parallelly. Other type of arborizations were the so-called astrocytic plates, which were frequently arranged at layers and embraced the elements of the neuropappila under the form of capsules. Multiple desmosomo-like and gap junctions were encountered between adjoining astrocytic membranes. Heterogenous astro-oligodendrocytic gap junctions were observed as well. The functional significance of these glial cells and their probable role in neuronal metabolism is discussed on the basis of a comparative analysis of the structural and ultrastructural characteristics of astrocytes in LOC of a pigeon and in various species of mammals.

Animals↗
PubMed1989

Dynamic morphological responses of mouse astrocytes in primary cultures following medium changes.

Within 5 minutes of changing the medium of 3-4 week old mouse astrocyte cultures, dramatic morphological alterations were seen in the cultures at the phase microscope level. These alterations included the appearance of membrane ruffles, followed by the formation of phase light vacuolar regions. Ultrastructurally, these ruffles could be seen as phagocytic arms, and the vacuoles appeared as blisters of the superficial cell layer. These morphological responses were due to the introduction of new serum proteins. Colloidal gold-labelled serum proteins were used to visualize the dynamics of the macromolecular uptake following this medium change. Some proteins were taken up by phagocytosis, whereas others were associated with coated vesicles and endosomal vesicles. The majority of these gold-labelled proteins were concentrated in vacuoles (presumably lysosomes) and were localized in the superficial cellular sheets. Inner cellular sheets contained little colloidal gold-labelled serum proteins, but displayed prominent pinocytotic profiles. Glucose consumption in these cultures remained constant at 1.6 mumoles/mg protein/hr. Glycogen content varied among individual cells, but it remained constant in the cultures at 60 nmoles bound glucose/mg protein throughout the 48 hour examination period. These results suggest that dense cultures of primary astrocytes may act similarly to the glia limitans.

Animals↗
PubMed1987

Morphological differentiation of cultured astrocytes is blocked by cadmium or cobalt.

The morphological transformation of astrocytes in primary culture from flat to process bearing is induced by cyclic adenosine monophosphate (cAMP). Calcium currents in cultured astrocytes are also enhanced by cAMP. This correlation suggests the hypothesis that cAMP-induced calcium entry causes the morphological differentiation. The experiments reported here show that cadmium or cobalt, which block astrocyte calcium channels, also block the cAMP-induced morphological differentiation. These results support the hypothesized link between calcium entry and astrocyte differentiation.

Animals↗
PubMed2005

Electrophysiological and morphological characterization of dentate astrocytes in the hippocampus.

We studied electrophysiological and morphological properties of astrocytes in the dentate gyrus of the rat hippocampus in slices. Intracellular application of Lucifer yellow revealed two types of morphology: one with a long process extruding from the cell body, and the other with numerous short processes surrounding the cell body. Their electrophysiological properties were either passive, that is, no detectable voltage-dependent conductance, or complex, with Na+/K+ currents similar to those reported in the Ammon's horn astrocytes. We did not find any morphological correlate to the types of electrophysiological profile or dye coupling. Chelation of cytoplasmic calcium ([Ca2+]i) by BAPTA increased the incidence of detecting a low Na+) conductance and transient outward K+ currents. However, an inwardly rectifying K+ current (Kir), a hallmark of differentiated CA1/3 astrocytes, was not a representative K+-current in the complex dentate astrocytes, suggesting that these astrocytes could retain an immature form of K-currents. Dentate astrocytes may possess a distinct current profile that is different from those in CA1/3 Ammon's horn.

Animals↗
PubMed1990

[Ultrastructural research on the sensorimotor cortex in adult rats. I. Intranuclear inclusions in the neurons and astrocytes].

The morphological peculiarities of neurones and astrocytes in the sensorimotor cortex of mature (over 3 months) and elderly (over 24 months) rats were studied at electron microscopic level. Intranuclear inclusions are found in the nuclei of pyramidal neurones from the third and fifth layer. On the basis of their fine structure they could be grouped into the following types: 1. Filamentous bundles. 2. Filamentous crystalloids. 3. Granulofilamentous bodies. 4. Membrane-enclosed inclusions. 5. Combined intranuclear inclusions. Filamentous crystalloids are found in two varieties, composed of filaments with various diameter and way of arrangement. Membrane-enclosed bodies are formed as small vesicles or large vacuoles. Combinations from various types of inclusions in the nucleus of a neurone are discovered frequently. Only intranuclear inclusions of the type of membrane-enclosed bodies are observed in the nuclei of astrocytes. These bodies are found only in the nuclei of astrocytes of elderly animals. On the basis of the comparative analysis between ultrastructural characteristics and frequency of intranuclear inclusions in pyramidal neurones and astrocytes in sensorimotor cortex of mature and elderly rats their probable connection with age changes in the central nervous system is discussed.

Aging↗
PubMed1990

Morphological arrangement between astrocytes and trigeminal mesencephalic primary afferent neurons in the rat.

The arrangement between astrocytes and the primary afferent neurons of the mesencephalic trigeminal nucleus (Me5) was analyzed in a light and electron microscopy immunocytochemistry study using anti-GFAP antibodies. It appears that each Me5 neuron is almost entirely sheathed with astrocytic processes radiating out from two or more astrocytes. Ultrastructural observations confirmed the embracement of Me5 neurons by astrocytic processes that only allowed some synaptic contacts on the neuronal surface. The possible functional significance of this intimate morphological relationship for the mesencephalic trigeminal neurons is discussed.

Animals↗
PubMed1986

Protein kinase C in astrocytes: a determinant of cell morphology.

Protein kinase C-like activity was found to be present in astrocytes prepared from rat neocortex and maintained in culture. Exposure to phorbol 12-myristate 13-acetate (PMA) caused a redistribution of this kinase from the cytosol to the membrane fraction of these cells. Also PMA was found to cause a profound change in astrocyte morphology; cells were converted from flat, polygonal, undifferentiated cells to process-bearing cells.

Animals↗