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PubMed1994

An immediate morphopathologic response of a subpopulation of astrocytes to electroshock: "dark" astrocytes.

Varying numbers of astrocytes lining the subarachnoid and Virchow-Robin's spaces become stainable by a special silver method in brain sections of rats subjected to a single electroshock of "suitable" parameters immediately before being sacrificed by perfusion fixation. This type of argyrophilia is considered to be induced by some electrically caused morphological damage, since the affected astrocytes are dramatically shrunken and hyperchromatic at both light- and electron-microscopic levels. Based on several points of morphopathologic similarity between the electroshock-damaged astrocytes and "dark" cells of various tissues, especially electroshock-induced "dark" neurons, it is supposed that their nature is also similar ("dark" astrocytes).

Animals↗

PubMed2001

Identification and characterization of uptake systems for cystine and cysteine in cultured astrocytes and neurons: evidence for methylmercury-targeted disruption of astrocyte transport.

Maintenance of appropriate intracellular glutathione (GSH) levels is crucial for cellular defense against oxidative damage. A suggested mechanism of methylmercury (MeHg) neurotoxicity implicates the involvement of oxygen radical formation and a decrease in cellular levels of GSH. Astrocytes play an important role in providing GSH precursors to neurons, and as will be discussed in this review, altered GSH homeostasis likely leads to impairment of astrocytic handling of glutamate, and neuronal energy metabolism. The review summarizes recent observations on transport systems for cysteine and cystine, precursors of GSH, in primary cultures of astrocytes and neurons, and their sensitivity to MeHg treatment.

Animals↗

PubMed1987

Preferential adhesion of brain astrocytes to laminin and central neurites to astrocytes.

Astrocytes from either fetal or newborn rat brain adhered preferentially to surfaces coated with active laminin. Neurites from septal neurons did not show a preference for active over inactive laminin. However, when given a choice between laminin and an astrocytic surface, septal cells preferred to extend neurites over astroglial processes. Hence, laminin paths can guide astrocyte migration, which, in turn, can guide neurite elongation.

Animals↗

PubMed1990

Astrocytes as antigen presenting cells for primary and secondary T cell responses: effect of astrocyte infection by murine hepatitis virus.

CD4+ T cell lines specific for murine hepatitis virus (MHV) - JHM or myelin basic protein (MBP) proliferated when cultured together with MHC class I and II positive syngeneic rat astrocytes and either inactivated virus or MBP as antigen. The magnitude of the T cell proliferative response was comparable to that seen when thymocytes were used as a source of antigen presenting cells (APC). In contrast, MHC class I and II positive astrocytes were unable to significantly stimulate the proliferation of highly purified populations of naive CD4+ and CD8+ T cells in an allogeneic mixed lymphocyte reaction (MLR). Both T cell populations proliferated when mixed with allogeneic lymph node cells. Infection of the astrocytes with a variant of MHV-JHM (PI-AS22D) did not alter this cells incapacity to stimulate the naive CD4+ and CD8+ T cells to proliferate.

Animals↗

PubMed1991

The action of calcitonin gene-related peptide on astrocyte morphology and cyclic AMP accumulation in astrocyte cultures from neonatal rat brain.

The actions of calcitonin gene-related peptide (CGRP) were investigated on 9- to 14-day-old astrocyte cultures obtained from the cerebra of 1- to 2-day-old rats. The morphological appearance of the cells was monitored by immunofluorescent staining of glial fibrillary acidic protein (GFAP), and the concentration of adenosine 3',5'-monophosphate (cyclic AMP) was measured in the cultures using radioimmunoassay. CGRP induced a morphological change in cultured astrocytes from rat brain. Flat, polygonal cells positive for GFAP became multipolar with many processes. In addition, CGRP stimulated the accumulation of cyclic AMP by up to 30-fold, half maximal stimulation being obtained at CGRP concentrations in the range 100-300 nM. These data provide evidence for the presence of functional CGRP receptors on astrocytes and suggest a role for CGRP as an intercellular messenger controlling the state of differentiation and activation of astroglial cells.

Animals↗

PubMed1993

Human astrocytes and cytokines: tumor necrosis factor alpha and interferon gamma do not promote astrocytic proliferation.

Astrocyte cell cultures were established from human fetal brains and exposed to human recombinant tumor necrosis factor alpha (TNF alpha) and human recombinant interferon gamma (IFN gamma), and the proliferative response was assessed by bromodeoxyuridine-immunostaining technique. TNF alpha showed an inhibitory activity, while IFN gamma induced a slight increase in the number of astrocytes undergoing cell division. However, in both experiments differences were not statistically significant. Previous studies have demonstrated that TNF alpha and IFN gamma are potent mitogens for adult astrocytes in both in vivo and in vitro conditions. Our results suggest that in developing brain the immunomodulatory activity of cytokines, TNF alpha and IFN gamma, is different from that observed in adult brain.

Astrocytes↗

PubMed1987

Organization of microfilaments in astrocytes that form in the presence of dibutyryl cyclic AMP in cultures, and which are similar to reactive astrocytes in vivo.

This paper deals with changes in the arrangement of microfilaments at various stages during the transformation of astroblasts into reactive astrocytes in the presence of dibutyryl 3',5'-cyclic adenosine monophosphate in vitro. When cultures of two-week-old mouse astroblasts are treated with dibutyryl cyclic AMP, drastic changes occur in cell shape and in the organization of microfilaments, resulting in cells that closely resemble reactive astrocytes in vivo. A thick, prominent ring of microfilaments in such cells which stains strongly with 7-nitrobenz-2 oxa-1,3-diazole-phallacidin, delineates the perikaryon. Electron microscope examination showed that the ring is composed of many smaller bundles of microfilaments running parallel to each other. Prominent bundles of microfilaments radiate from the cell body into the cell processes. Based on the observation of intermediate forms, we propose that the microfilament ring may be important in the development of cell processes in reactive astrocytes.

Actin Cytoskeleton↗

PubMed2004

Oxidized low-density lipoprotein is present in astrocytes surrounding cerebral infarcts and stimulates astrocyte interleukin-6 secretion.

Ischemic injury to brain is associated with both disruption of the blood-brain barrier and increased oxidative stress. Given the neurotoxicity associated with exposure to oxidized low-density lipoprotein (oxLDL) in vitro, we tested the hypothesis that oxLDL may be present in parenchymal cells of cerebrum after infarction and that oxLDL may influence the pathophysiology of cerebral infarction. Our results showed that the subacute phase of cerebral infarction in patients was characterized by the appearance of oxLDL epitopes in astrocytes, but not neurons or microglia, in the perinecrotic zone. We further demonstrated that minimally oxLDL was most effectively internalized by primary cultures of rat astrocytes, and that exposure to minimal oxLDL stimulated astrocyte interleukin-6 secretion but did not alter nitric oxide production. These results demonstrate for the first time that oxLDL is present in brain parenchyma of patients with ischemic infarction and suggest a potential mechanism by which oxLDL may activate innate immunity and thereby indirectly influence neuronal survival.

Adult↗

PubMed1998

Functional IL-4 receptors on mouse astrocytes: IL-4 inhibits astrocyte activation and induces NGF secretion.

IL-4 is a Th2-derived cytokine which plays an important role in the function of various immunocompetent cells as well as in the pathophysiology of various CNS disorders. In this study we characterized the expression of IL-4R in cultured astrocytes and explored the effects of IL-4 on the function of these cells. We found that astrocytes express the mRNA of both the membrane-bound and the soluble forms of the IL-4R, whereas they do not secrete IL-4. IL-4 inhibited both NO production and iNOS expression induced by LPS stimulation and decreased the secretion of TNF-alpha and the expression of ICAM-1. In contrast, IL-4 induced the secretion of NGF by astrocytes and synergized with LPS and TNF-alpha in this effect. These results suggest an important role for IL-4 as an immunosuppressive and a neurotrophic factor in the CNS.

Animals↗

PubMed2001

Dual growth arrest pathways in astrocytes and astrocytic tumors in response to Raf-1 activation.

Normal human fibroblasts have been shown to undergo a p16(Ink4a)-associated senescence-like growth arrest in response to sustained activation of the Ras/Raf/MEK/ERK pathway. We noted a similar p16(Ink4a)-associated, senescence-like arrest in normal human astrocytes in response to expression of a conditional form of Raf-1. While HPV16 E7-mediated functional inactivation of the p16(Ink4a)/pRb pathway in astrocytes blocked the p16(Ink4a)-associated growth arrest in response to activation of Raf-1, it also revealed a second p21(Cip1)-associated, senescence-associated, beta-galactosidase-independent growth arrest pathway. Importantly, the p21(Cip1)-associated pathway was present not only in normal astrocytes but also in p53-, p14(ARF)-, and p16(Ink4a)/pRb-deficient high grade glioma cells that lacked the p16(Ink4a)-dependent arrest mechanism. These results suggest that normal human cells have redundant arrest pathways, which can be activated by Raf-1, and that even tumors that have dismantled p16(Ink4a)-dependent growth arrest pathways are potentially regulated by a second p21(Cip1)-dependent growth arrest pathway.

Astrocytes↗

PubMed1991

C6 glioma-astrocytoma cell and fetal astrocyte migration into artificial basement membrane: a permissive substrate for neural tumors but not fetal astrocytes.

Cortically homografted C6 glioma-astrocytoma cells both invade the rat host brain as a mass and migrate as individual cells. In contrast, fetal astrocytes derived from homografted whole pieces of fetal cortex migrate only as individual cells throughout the brain of the rat but are not capable of invasion. Our experiment explored the migratory capacity (over 7 days) of cultured purified fetal astrocytes and C6 cells after seeding 10(6) cells on a hydrated artificial basement membrane wafer (Matrigel). The artificial basement membrane wafer was not a suitable substrate for the growth of cultured fetal astrocytes. In contrast, C6 cells migrated as individual cells from the surface of the wafer into the substrate. Individual C6 cells migrated 1.8 mm in the first 4 days and then ceased migration. The C6 cells were observed at the base of a digestion tube that extended from and was open to the surface of the wafer. At 3 days, micropockets were observed to form around each C6 cell at the base of each tube. By 7 days, the majority of pockets observed were large and contained several C6 cells. These multiple cell groups appeared to be progenitors of tumor masses. These data indicate that C6 glioma-astrocytoma cells, which in vivo appear to be a model for glioblastoma multiforme, primarily migrate as individual cells through artificial basement membrane and secondarily form tumor masses. Progenitor tumor masses form by coalescence of individual C6 cell micropockets or the division of a single cell in an individual micropocket.

Animals↗

PubMed1982

Ultrastructural study of enzymes in reactive astrocytes: clarification of astrocytic activity.

Enzymes in reactive of the cerebral cortex were examined at the ultrastructural level in an attempt to resolve some conflicting aspects of astrocytic activity. Correlations between morphological and enzyme changes after injury established that the apparent increase in oxidative enzyme activity was exclusively mitochondrial and not an artefactual reaction product resulting from anoxic cellular damage. Pronounced glucose-6-phosphatase activity within cisternae of an increased amount of the granular endoplasmic reticulum was related to increased glycogen. Further evidence from acid phosphatase activity indicated that astrocytes played a minimal role in phagocytosis.

Acid Phosphatase↗

PubMed2004

Frontotemporal dementia with co-occurrence of astrocytic plaques and tufted astrocytes, and severe degeneration of the cerebral white matter: a variant of corticobasal degeneration?

We report two patients who exhibited frontotemporal dementia (FTD) with unusual neuropathological features. The ages of the patients at death were 65 and 67 years, the disease durations were 6 and 5 years, and the clinical diagnoses were Pick's disease and corticobasal degeneration (CBD), respectively. At autopsy, both cases exhibited neuropathological findings compatible with those of CBD, including atrophy of the frontal and parietal lobes, neuronal loss and gliosis in the cortical and subcortical regions, and presence of cortical ballooned neurons and astrocytic plaques (APs). In both cases, immunoblotting of insoluble tau exhibited the pattern of selective accumulation of four-repeat tau, a finding that is also compatible with CBD. However, severe degeneration was evident in the frontal and parietal white matter in both cases. Moreover, a striking finding was the widespread presence in the affected cortex of tufted astrocytes (TAs), which are characteristic of progressive supranuclear palsy (PSP). Neither co-occurrence of APs and TAs nor severe degeneration of the cerebral white matter is a feature of either CBD or PSP. No mutations were found in the tau gene in either case. In conclusion, the possibility that these two cases represent a new neuropathological phenotype of non-familial FTD rather than simply a variant of CBD cannot be completely excluded.

Amyloid beta-Peptides↗

PubMed2005

The blockade of endothelin A receptor protects astrocytes against hypoxic injury: common effects of BQ-123 anderythropoietin on the rejuvenation of the astrocyte population.

In the present study the role of endothelin (ET) and its receptors (ETA-R and ETB-R) in cellular mechanisms underlying the resistance of astroglial cells to low oxygen level and development of hypoxia has been investigated. To define the influences of ET and its receptors on survival and on antigenic as well as morphologic differentiation of rat astroglial cells in normoxic (NC) and hypoxic culture (HC) the selective antagonists of ETA-R (BQ-123) and ETB-R (BQ-788) were used. Treatment of HC with BQ-123 caused an increase in cell number and inhibited the hypoxia-induced apoptosis by 37%. BQ-123 decreased the hypoxia-induced cytotoxicity in HC. These effects of BQ-123 were abolished in cultures simultaneously treated with BQ-123 and BQ-788. Administration of BQ-788 alone decreased the number of living cells in NC, but not in HC. The activity of caspase-3/-7 was not changed by exposure of NC and HC to BQ-788. The protection provided by BQ-123 to astroglial cells against cytotoxicity in NC and HC was similar to that of erythropoietin (EPO), a cytokine with established neuroprotective effects. The functional improvement of astroglial cells and slowing down of their differentiation under exposure to BQ-123, or EPO, or BQ-123 + EPO has been evidenced by an increased number of nestin+/glial fibrillary acidic protein-positive (GFAP+) astrocytes accompanied by decrease of nestin-/GFAP+ cells. The simultaneous treatment with BQ-123 and EPO additionally decreased the activities of caspase-3/-7 (64%) and release of LDH into the medium (94%). The benefits in the functional states of astrocytes obtained by combined treatment of HC with BQ-123 and EPO suggest a new therapeutic strategy in treatment of hypoxic brain injury.

Animals↗

PubMed2002

Dorsal root rupture injury induces extension of astrocytic processes into the peripheral nervous system and expression of GDNF in astrocytes.

Preganglionic brachial plexus injuries fall into two categories according to the lesion site, root avulsion injury and root rupture injury. The latter type of injury involves part of the peripheral nervous system (PNS) component at the injured spinal cord surface. Previous investigators have used rhizotomy of experimental animals as a model for dorsal root rupture injury. However, the effect on the central nervous system (CNS)-PNS junction accompanied by the mechanical stress from traction force is hard to estimate in this model. The current study aimed to demonstrate temporal molecular alterations from the CNS-PNS junction to the ruptured dorsal root after traction injury by immunohistochemical procedures. At 28 days after dorsal rupture injury, GFAP-positive structures could be clearly identified showing rather straight lines from the centro-peripheral junction toward the peripheral stump in the ruptured dorsal root. Immunoelectron microscopy for GFAP verified GFAP IR within the astrocytic processes at the injured dorsal root at 28 days after dorsal rupture injury. Glial cell line-derived neurotrophic factor immunoreactivity (GDNF IR) was slightly upregulated within the Schwann cell bodies on the injured dorsal root at 24-48 h after rupture injury. However, GDNF IR had appeared showing a process-like profile on the ruptured dorsal root by 28 days, and it was closely related with GFAP-positive structures. In contrast, a small increase in GFAP IR was only detected on the proximal side on the rhizotomized dorsal root at 28 days after rhizotomy. A marked decrease in NF IR and S-100 IR was observed at the ruptured dorsal root from 7 days. On the other hand, laminin IR was strongly upregulated on the ruptured dorsal root from 48 h to 7 days, and was still evident at 28 days. We therefore conclude that the astrocytes show a unique ability to extend their processes toward the stump. This ability may provide a new medium for the study of axonal regeneration in future clinical experiments.

Animals↗

PubMed1998

A novel metabolic communication between neurons and astrocytes: non-essential amino acid L-serine released from astrocytes is essential for developing hippocampal neurons.

A hippocampal astrocyte conditioned medium (HACM) supported the survival of hippocampal neurons under a serum-, glia-free culture setting. The neurotrophic activity in HACM was mostly recovered in low molecular weight fractions (Mr < 3000), which contained high levels of L-serine and L-alanine. However, L-serine alone significantly improved the neuronal survival and neurite growth in a stereo-specific manner. Other non-essential amino acids had no effect. These results strongly suggest that L-serine, released by astrocytes, is essential for the survival and phenotypic growth of hippocampal neurons.

Animals↗

PubMed1996

Metabolism of [U-13C5] glutamine in cultured astrocytes studied by NMR spectroscopy: first evidence of astrocytic pyruvate recycling.

Metabolism of [U-13C5]glutamine was studied in primary cultures of cerebral cortical astrocytes in the presence or absence of extracellular glutamate. Perchloric acid extracts of the cells as well as redissolved lyophilized media were subjected to nuclear magnetic resonance and mass spectrometry to identify 13C-labeled metabolites. Label from glutamine was found in glutamate and to a lesser extent in lactate and alanine. In the presence of unlabeled glutamate, label was also observed in aspartate. It could be clearly demonstrated that some [U-13C5]glutamine is metabolized through the tricarboxylic acid cycle, although to a much smaller extent than previously shown for [U-13C5]glutamate. Lactate formation from tricarboxylic acid cycle intermediates has previously been demonstrated. It has, however, not been demonstrated that pyruvate, formed from glutamate or glutamine, may reenter the tricarboxylic acid cycle after conversion to acetyl-CoA. The present work demonstrates that this pathway is active, because [4,5-13C2]glutamate was observed in astrocytes incubated with [U-13C5]-glutamine in the additional presence of unlabeled glutamate. Furthermore, using mass spectrometry, mono-labeled alanine, glutamate, and glutamine were detected. This isotopomer could be derived via the action of pyruvate carboxylase using 13CO2 produced within the mitochondria or from labeled intermediates that had stayed in the tricarboxylic acid cycle for more than one turn.

Alanine↗

PubMed2005

Development of GLAST(+) astrocytes and NG2(+) glia in rat hippocampus CA1: mature astrocytes are electrophysiologically passive.

Glia show marked heterogeneity in terms of electrophysiology in the developing brain, and two major types can be identified based on GFAP or NG2 expression. However, it remains to be determined if such an electrophysiological diversity holds for the adult brain and how GFAP and NG2 lineage glia are associated with different electrophysiological phenotypes during the course of development. To address these fundamental questions, we performed in situ whole cell recording from morphologically identified glia from the rat hippocampal CA1 region from postnatal (P) days 1-106 and double-stained postrecorded cells with GLAST and NG2 antibodies. We found glia express mostly voltage-gated outward K(+) currents and also have inward Na(+) currents in the newborn (P1-P3), but these are no longer present after P22. They consist equally of GLAST(+) and NG2(+) cells in the newborn, but are mainly NG2(+) in juvenile animals (P4-P21). Glia showing voltage-gated outward and inward K(+) currents are also present at P1, peak at P5 and decline to a stationary level of approximately 10% in the adult. They are GLAST(+) astrocytes from newborn to juvenile but NG2(+) glia in the adult. Electrophysiologically passive glia first appear at P4 and increase to 91% in adults, of which 85% are GLAST(+). These results indicate that glial electrophysiological diversity occurs predominantly in the developing brain. While most glia in the NG2 lineage preserve a certain amount of voltage-gated ion conductances, mature GLAST(+) astrocytes are electrophysiologically passive.

Action Potentials↗