Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Astrocyte morphology”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

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

At least 109 records · Page 6Linked to original sources
PubMed2004

Reversible disruption of tight junction complexes in the rat blood-brain barrier, following transitory focal astrocyte loss.

Breakdown of the blood-brain barrier is a feature of acute and chronic neurodegenerative changes, yet the relationship between astrocytes and the mature barrier remains unclear. We studied this role of astrocytes in vivo using a gliotoxin and evaluated changes in three vascular tight junction markers. Male Fisher F344 rats given systemic 3-chloropropanediol showed astrocytic loss in the inferior colliculus from 12-24 h until the lesion was repopulated 8-28 days later. Within 6 h of astrocyte loss, microvessels in this area began to demonstrate a loss of the normal paracellular localization of the transmembrane proteins occludin and claudin-5 and cytoplasmic zonula occludens-1, which correlated with focal vascular leak of dextran (10 kDa) and fibrinogen. Platelet endothelial adhesion molecule-1 staining revealed that there was no loss of the endothelial lining. Between 4-8 days, severe downregulation of tight junction protein expression was observed, which subsequently returned over the same time period as astrocytes repopulated the lesion. Unexpectedly, dextran and fibrinogen leak from vessels had ceased at 6 days, well before the return of occludin and claudin-5 to appropriate paracellular domains. Control nonvulnerable cortical tissue showed no change in astrocyte morphology and tight junction expression over the same time course. Our data supports a primary role for astrocytic contact in the expression of occludin, claudin-5, and zonula occludens-1 in the mature brain vasculature in vivo. However, barrier integrity to dextran (10 kDa) and fibrinogen can be restored in the absence of astrocytes and tight junction proteins (occludin, claudin-5, and zonula occludens-1).

Animals↗
PubMed1999

Endothelins stimulate expression of cyclooxygenase 2 in rat cultured astrocytes.

Endothelin (ET) is one of the active endogenous substances regulating the functions of astrocytes. In the present study, we examined effects of ET on cyclooxygenase (COX) expression in cultured astrocytes. ET-3 (100 nM) caused transient increases in the expression of both COX2 mRNA and protein, but not those of COX1, in cultured astrocytes. ET-induced COX2 mRNA expression was suppressed by 5 microg/ml actinomycin D, 30 microM BAPTA/AM, inhibitors of protein kinase C (1-100 nM staurosporin and 100 microM H-7), 2 microM dexamethasone, and prolonged treatment with 100 nM phorbol 12-myristate 13-acetate. ET-3 stimulated production of prostaglandin (PG) E2 in cultured astrocytes. The effect of ET-3 on the PGE2 production was diminished by actinomycin D. Indomethacin and NS398, a selective COX2 inhibitor, comparably decreased both the basal and the ET-stimulated PGE2 production. Proliferation of cultured astrocytes was stimulated by 100 nM ET-3, and the increased proliferation was reduced by co-addition of 1 microM PGE2. Treatment with 1 microM PGE2 caused astrocytic morphological changes accompanied by disappearance of stress fibers, a prominent structure of organized cytoskeletal actin in cultured astrocytes. In the presence of 10 nM ET-3, PGE2 did not show an effect on astrocytic actin organization. The present study shows that ET is an inducer of astrocytic COX2 and suggests that ET-induced PGE2 production through COX2 may be involved in the regulation of astrocytic functions.

Animals↗
PubMed1992

Effect of dibutyryl cyclic AMP-treatment on prostaglandin F2 alpha-stimulated phosphoinositide hydrolysis in cultured rat astrocytes.

Dibutyryl cyclic AMP (dBcAMP)-treatment of cultured rat astrocytes induced changes in astrocyte morphology followed by the potentiation of prostaglandin F2 alpha (PGF2 alpha)-stimulated phosphoinositide (PI) hydrolysis. The potentiation was observed in astrocytes of the cerebral cortex, cerebellum, and hippocampus. The dBcAMP-treatment induced agonists-specific changes in PI hydrolysis; e.g., the potentiation of norepinephrine-effect and the reduction of the carbachol-effect. Coincubations of carbachol or norepinephrine with PGF2 alpha produced additive responses.

Animals↗
PubMed1998

Vitamin E induces ramification and downregulation of adhesion molecules in cultured microglial cells.

Microglial cells in the healthy adult CNS possess a characteristic ramified morphology and show little or no expression of major histocompatibility complex (MHC) or adhesion molecules. In contrast, microglial cells isolated from newborn rat brains inevitably show a nonramified amoeboid morphology and express immunoeffector molecules, such as MHC class I and II, and various adhesion molecules thought to be markers of microglial activation. Furthermore, they produce large amounts of oxygen radicals. Treatment of cultured microglial cells with the antioxidants vitamin E (alpha-tocopherol) and vitamin C (ascorbic acid) induced a ramified microglial morphology after 48 h in vitro, otherwise only seen in healthy adult CNS tissue or in co-culture with astrocytes. Morphological transformation of microglial cells was quantified by morphometric analysis and was found to be statistically significant. Ramification of microglia induced by vitamin E was accompanied by downregulated expression of adhesion molecules leukocyte function antigen-1, very late antigen-4, and intercellular adhesion molecule-1, as assessed by FACS analysis and immunocytochemistry. Moreover, cell numbers of microglia treated with vitamin E remained stable within 7 days in vitro, whereas untreated controls showed a cell loss of 81.5%. These data show that vitamin E acts as a protective compound in dissociated microglial cell cultures. In conclusion, our results suggest that vitamin E and vitamin C shift microglial morphology toward ramification and induce an immunological deactivation. These changes seem to be mediated by oxidative mechanisms.

Animals↗
PubMed2005

Time course changes of estrogen receptor alpha expression in the adult rat hippocampus after kainic acid-induced status epilepticus.

Although estrogens possess neuroprotective and epileptogenic properties, the expression pattern of the estrogen receptor (ER) following status epilepticus (SE) remains unclear. We therefore examined the expression pattern of ER alpha in the adult rat hippocampus after SE. SE was induced in rats by kainic acid (KA; 12 mg/kg, i.p.). ER alpha expression was assessed by immunostaining and Western blotting at various times (24 h, and 7, 14, and 21 days) after SE onset. Immunohistochemistry disclosed ER alpha expression in the CA1 and CA3 pyramidal cells of control rats, whereas, after SE, ER alpha-immunoreactive neurons decreased in number due to neuronal death in the CA1 from days 7 to 21. On the other hand, ER alpha-immunoreactive cells with astrocytic morphology were observed in the CA1 beginning on day 7 after SE. This immunoreactivity increased in proportion to the hypertrophy of astrocytes up to day 21. Western blotting revealed a significant decrease in ER alpha expression on day 7 after SE in comparison with control level. However, ER alpha expression on days 14 and 21 were similar when comparing KA-treated and control rats. These results indicate that reactive astrocytes are important sites of estrogen action in the hippocampal CA1 after SE.

Animals↗
PubMed2004

Combined effects of ammonia and manganese on astrocytes in culture.

Ammonia has been strongly implicated in the pathogenesis of hepatic encephalopathy (HE), and astrocytes appear to be the primary target of ammonia neurotoxicity. Recent work has shown that manganese also plays a role in the pathogenesis of HE and causes astrocyte morphologic and functional changes similar to ammonia. We therefore investigated whether a combination of these compounds could produce additive/synergistic effects. Cultured astrocytes treated with 5 mM ammonia (NH4Cl) along with 100 microM manganese acetate (MnAc) for 3 h showed a 55-65% increase in free radical production over ammonia or manganese alone (P < 0.05). There was also a 50% decrease in the mitochondrial membrane potential (beta psi(m)) at 24 h following treatment with NH4Cl (5 mM) plus MnAc (50 microM) (P < 0.05), as compared to ammonia or manganese alone. Astrocytes treated with ammonia or manganese alone for 24 h showed no cell death, as determined by LDH release and light microscopic examination. However, cultures treated with ammonia plus manganese showed 80-90% necrotic cell death as estimated by light microscopy and 59% cell death as determined by LDH release. LDH release by ammonia plus manganese was blocked by the antioxidant superoxide dismutase (25 units/ml) as well as by the nitric oxide synthase inhibitor N(omega)-nitro-L-argininemethyl ester (500 microM). In conclusion, ammonia plus manganese exert additive/synergetic effects on the induction free radicals, mitochondrial inner membrane depolarization and cellular integrity, which may contribute to the tissue injury associated with chronic forms of HE.

Ammonia↗
PubMed2000

Immunocontent and secretion of S100B in astrocyte cultures from different brain regions in relation to morphology.

Primary astrocyte cultures prepared from neonatal hippocampus, cerebral cortex and cerebellum were morphologically distinct. Cells from hippocampus and cortex were almost entirely protoplasmic, whereas cerebellar astrocytes had many processes; in the absence of serum these differences were accentuated. We compared the immunocontent and secretion of the mitogenic protein S100B in these cultures. Immunocontent was 2.5 times higher in cerebellar astrocytes than in hippocampal or cortical astrocytes. Cells from all three regions secreted S100B under basal conditions, but the secretion rate was higher in cerebellar astrocytes. Secretion depended on protein synthesis and was increased by incubation with forskolin or lysophosphatidic acid in mechanisms which were additive. The stellate morphology induced by forskolin was reversed by lysophosphatidic acid in hippocampal but not in cerebellar cultures, suggesting that S100B secretion was not associated with a process-bearing phenotype of astrocytes.

Animals↗
PubMed1990

Fibronectin involvement following herpes simplex infection of cultured rat astrocytes.

To evaluate the potential impact of a strongly neurotropic virus on the matricial fibronectin (FN) of a given neural cell type, first subculture of rat astrocytes were inoculated with either a low (0.1-0.5) or a high MOI (10-100) of Herpes simplex virus-type 1 (HSV-1). Infected samples, as well as matched controls, were harvested from 12 to 72 h post-inoculation and processed for extracellular FN labeling by the peroxidase-antiperoxidase (PAP) method. Following low MOI, multinucleated cell formation and syncytial development drastically modified peripheral FN, since the typical loose network was largely replaced by a patch-like appearance. At high MOI, when viral action caused further cytoplasmic retraction leading to rounded or stellate cells, the FN pattern was remarkably altered, even with total FN loss around highly retracted cells. It may be concluded that a virus such as HSV-1, capable of modifying astrocyte morphology, induces a redistribution or loss of pericellular FN.

Animals↗
PubMed1991

Astrocyte expression of major histocompatibility complex gene products in multiple sclerosis brain tissue obtained by stereotactic biopsy.

Major histocompatibility complex (MHC) class I and class II antigens were characterized by immunocytochemistry in two chronic-active multiple sclerosis lesions in tissue obtained from two patients by stereotactic biopsy. We examined in particular astrocytic MHC-positive cells in relation to lesion architecture. The MHC class I (HLA-A,B,C)-positive astrocytic cells were widely dispersed, being present at the lesion edge, in the gliotic lesion center, and in normal-appearing white matter as well. Morphologically astrocytic MHC class II (HLA-DR)-positive cells were confined exclusively to the lesion edge. By staining serial sections with antisera to glial-fibrillary acidic protein and HLA-DR, we confirmed the lineage of several MHC class II-positive astrocytes. The demonstration of MHC antigen-positive astrocytes in multiple sclerosis tissue obtained by stereotactic biopsy is novel; the differential distribution of MHC class I- and class II-positive astrocytes in the multiple sclerosis lesion may provide suggestive clues about the regulation of MHC expression on these cells in vivo.

Adolescent↗
PubMed2003

A transgenic mouse model for the detailed morphological study of astrocytes.

We have generated a transgenic mouse model in which astrocytes express an enhanced green fluorescent protein (EGFP) under the control of the mouse glial fibrillary acidic protein (GFAP) promoter. EGFP, which is characteristically found throughout the cell, was expressed in these animals even in astrocytic fine processes, and EGFP expressing cells demonstrated morphological characters of protoplasmic, fibrous, or reactive astrocytes. In contrast, GFAP immunoreactivity was found only in the perinuclear region and in the main processes. The transgenic mouse model therefore provides a valuable tool for the detailed morphological investigation of astrocytes.

Animals↗
PubMed2000

In vivo expression of the interleukin 4 receptor alpha by astrocytes in epilepsy cerebral cortex.

We reported previously that non-neoplastic astrocytes (derived from brain tissues of patients with epilepsy) expressed interleukin 4 receptor alpha (IL-4Ralpha) and responded to interleukin 4 (IL-4) in culture. To determine whether reactivity of cultured astrocytes was relevant to primary tissue, we investigated IL-4Ralpha expression in specimens of non-neoplastic cerebral cortex removed for surgical treatment of intractable epilepsy compared to specimens of glial tumours, which have been reported to contain IL-4Ralpha. Freshly frozen tissues from eight cases (four epilepsy, four malignant astrocytoma) were evaluated for IL-4Ralpha expression by reverse-transcriptase polymerase chain reaction (RT-PCR), Southern blotting, and double-labelled immunohistochemistry with antibodies to IL-4Ralpha and glial fibrillary acidic protein (GFAP). IL-4Ralpha mRNA was detectable in both non-neoplastic and neoplastic tissues, whereas interleukin 2 receptor gamma chain (IL-2Rgammac) mRNA was not found. By immunohistochemistry, IL-4Ralpha protein co-localized to cells displaying GFAP and astrocytic morphology in epilepsy tissues. As anticipated, IL-4Ralpha was detectable in astrocytoma, but, surprisingly, was also observed in GFAP-positive, non-neoplastic "reactive" astrocytes adjacent to tumour. Results are consistent with the concept that non-neoplastic epilepsy astrocytes express IL-4Ralpha in situ, thus confirming in vitro studies and implying IL-4 sensitivity in vivo.

Actins↗
PubMed1998

Glial cells have heart: rH1 Na+ channel mRNA and protein in spinal cord astrocytes.

Astrocytes in vitro express several distinct voltage-sensitive sodium currents, including tetrodotoxin (TTX)-resistant in non-stellate astrocytes and TTX-sensitive currents in stellate astrocytes. However, the molecular identity of the underlying channels, and the mechanisms that regulate their expression, have yet to be identified. Since spinal cord astrocytes in vitro express sodium currents that are nearly ten-fold greater that those of astrocytes derived from other regions, we used reverse transcription polymerase chain reaction (RT-PCR), in situ hybridization, and immunocytochemistry to search for a sodium channel mRNA and protein corresponding to a TTX-resistant channel in these cells. RT-PCR did not detect transcripts for SNS, which is known to encode a TTX-resistant current in dorsal root ganglion neurons. However, RT-PCR demonstrated the presence of rH1 mRNA in cultured spinal cord astrocytes derived from postnatal day 0 (P0) Sprague Dawley rats at 7 days in vitro and in also intact spinal cords of P0 and P7 rats. Hybridization signal for rH1 mRNA was detected by in situ hybridization cytochemistry in most non-stellate and, at varying levels, in stellate astrocytes in these cultures. Immunocytochemical studies, utilizing a polyclonal antibody (R-12) generated against a conserved polypeptide sequence of sodium channels, demonstrated sodium channel immunoreactivity in non-stellate and stellate astrocytes in these cultures. Spinal cord cultures reacted with a rH1-specific polyclonal antibody also showed rH1 immunostaining in non-stellate and stellate astrocytes, although the intensity of the rH1 immunoreactivity in both astrocyte morphologies was attenuated compared to that observed with the R-12 generic sodium channel antibody. The presence of rH1 mRNA and protein in non-stellate astrocytes in vitro provides a possible correlate for the TTX-resistant current that has been recorded in these cells. Since TTX-resistant current is not present in stellate astrocytes, the presence of rH1 mRNA and protein in these cells suggests, in addition, that post-translational mechanisms participate in the control of sodium channel expression in these cells.

Animals↗
PubMed2006

Morphological interrelationship between astrocytes and nerve endings in the rat spinal trigeminal nucleus caudalis.

It has been reported that the spinal trigeminal nucleus caudalis (Sp5C), which receives nociceptive information from the oro-facial regions, has four laminae. To clarify the role of glial cells in the transmission of the nociceptive information, the present study was conducted to examine the detailed distribution of astrocytes in each lamina and also to investigate a morphological interrelationship between the astrocytes and nerve endings in the rat Sp5C. After the preparation of the serial cryostat sections, immunohistochemistry for glial fibrillary acidic protein (GFAP) was employed to identify the astrocytes, and immunohistochemistry for substance P (SP), calcitonin gene-related peptide (CGRP), was used for the nerve endings. We also employed double-labeling immunofluorescence and electron microscopic immunohistochemistry for the GFAP/SP or GFAP/CGRP. GFAP-positive reactions were observed in all laminae of the Sp5C, and SP- or CGRP-positive nerve endings were observed in the lamina I and II. Additionally, we clarified the presence of GFAP/SP- or GFAP/CGRP-positive reactions by the double-labeling immunofluorescence and demonstrated the morphological interrelationship between the astrocytes and nerve endings by the double-labeling electron microscopic immunohistochemistry. These findings suggest that astrocytes might play some roles in the transmission of nociceptive information from the oro-facial region.

Animals↗
PubMed2001

Rapid morphological changes in astrocytes are accompanied by redistribution but not by quantitative changes of cytoskeletal proteins.

Astrocytes have the potential to acquire very different morphologies, depending on their regional location in the CNS and on their functional interactions with other cell types. Morphological changes between a flat or a fibroblast-like and a stellate or process-bearing appearance, and vice versa, can occur rapidly, but very little is known as to whether morphological transformations are based on quantitative changes of cytoskeletal proteins in microfilaments, intermediate filaments, and/or microtubules. Using a cell culture of selective type 1 astrocytes, we compared the distribution and protein amounts of a number of cytoskeletal proteins both during primary process growth induced by specific media conditions and after secondary transformations induced by dBcAMP. Our data presented in this report support the idea that astrocytes can undergo dramatic changes in their morphology requiring subcellular redistribution of most cytoskeletal proteins but no quantitative modifications of the amount of the respective proteins. After pharmacological treatment with lysophosphatic acid and genistein we show that astrocytes can acquire intermediate morphologies reminiscent of both fibroblast and stellate-like cells. These experiments demonstrate that the recently described RhoA-mediated signaling cascade between the cell surface and cytoskeletal proteins is only one of several signaling pathways acting on the astrocytic cytoskeleton.

Actinin↗
PubMed1991

Endothelin induces a sustained rise in intracellular calcium in hippocampal astrocytes.

We report that the endothelins, a newly described family of vasoactive peptides, have a profound effect on intracellular calcium levels of cultured rat hippocampal astrocytes that resembles the effect of endothelin (ET) on vascular smooth muscle cells (VSMCs) in many respects. The astrocyte's response has two components that can be distinguished by their extracellular calcium requirement and time course. Within seconds of application, ET induces a transient calcium spike that corresponds to a release of calcium from internal stores. The second component follows immediately, is dependent upon extracellular calcium, and maintains an elevated intracellular calcium level for many minutes. Sustained elevations of intracellular calcium can dramatically alter astrocyte morphology and induce cell division in many other cell types. ET may serve these functions, and thus form a communication link between blood vessels and neurons through astrocytes.

Animals↗
PubMed1995

Astrogliosis in culture. IV. Effects of basic fibroblast growth factor.

Previous studies have shown that the mechanical wounding of 3-week-old cultured rat astrocytes results in cell proliferation and hypertrophy resembling astrocyte responses to a brain injury in vivo. We now report the effects of basic fibroblast growth factor (bFGF) and an anti-bFGF antibody on astrocyte morphology, proliferation, and migration following in vitro wounding of confluent secondary cultures. Addition of bFGF (20 ng/ml) to wounded cultures induced morphological changes characteristic of differentiation in wounded and nonwounded areas of the culture. Combined treatment with bFGF and an anti-bFGF antibody (100 micrograms/ml) prevented this effect. Astrocyte proliferation along the edges of a scratch wound was at maximum 24 hr after wounding in cells growing in Eagle's minimum essential medium (EMEM) containing 10% serum. Low serum concentration and treatment with dibutyryl cyclic adenosine monophosphate (dbc-AMP) reduced injury-associated astrocyte proliferation. Addition of bFGF to cultures in EMEM with serum increased astrocyte proliferation at 18 and 24 hr after wounding. This effect was reduced considerably by treatment of cultures with bFGF in combination with an anti-bFGF antibody. The combined treatment and the antibody alone reduced cell division to a level lower than in control cultures. Twenty-four hr following wounding, astrocytes along the edges of the wound exhibited extension of thick, flat processes into the wound area. At 3 and 5 days after wounding, a bodily migration of astrocytes into the wounded area was observed. Addition of bFGF significantly increased astrocyte migration 1 day after wounding, with maximum effect on day 3 and no subsequent increase on day 5. A combination of bFGF and anti-bFGF antibody as well as the antibody alone reduced astrocyte migration to a level lower than in controls. Immunohistochemical localization and isoform pattern of bFGF in astrocytes did not change with dbc-AMP treatment or wounding. We conclude that mechanically wounded confluent astrocytes respond to bFGF added to the culture medium by enhancing cell division, differentiation, and migration. In addition, the results of the antibody treatment also suggest a role for endogenous bFGF in astrocyte proliferation and migration elicited by wounding in vitro. These results support the notion that in vivo, both bFGF released by injury and endogenous bFGF synthesized by astrocytes, contribute to the cellular responses that lead to astrogliosis.

Animals↗
PubMed2004

Involvement of the S100B in cAMP-induced cytoskeleton remodeling in astrocytes: a study using TRTK-12 in digitonin-permeabilized cells.

1. Stellation of astrocytes in culture involves a complex rearrangement of microfilaments, intermediate filaments, and microtubules, which reflects in part the plasticity of these cells observed during development or after injury. 2. An astrocytic calcium-binding protein, S100B, has been implicated in the regulation of plasticity due to its ability to interact with cytoskeletal proteins. 3. We used digitonin-permeabilized astrocytes to introduce TRTK-12, a peptide that binds to the C-terminal of S100B and blocks its interaction with cytoskeletal proteins. 4. TRTK-12 was able to block cAMP-induced astrocyte stellation and this effect was dependent on the concentration of the peptide. These results support the idea that S100B has a modulatory role on astrocyte morphology.

Animals↗
PubMed1993

Multiple restricted lineages in the embryonic rat cerebral cortex.

We have labelled precursor cells in the embryonic rat cerebral cortex using BAG, a retroviral vector that expresses beta-galactosidase. We had previously reported that labelled precursor cells generate clusters of labelled cells that could be classified into four types by their morphological appearance and anatomical distribution (Price and Thurlow, 1988). In this study, we have used immunohistochemistry and intracellular dye labelling to identify the cell types that make up these clusters. We discovered that clusters are almost always composed of a single cell type. In addition to clusters composed entirely of neurones, we found four different types of glial cell clusters. In the grey matter, glial clusters are composed either of protoplasmic astrocytes, or of cells that have an astrocyte morphology, but no glial filaments. In the white matter, clusters are composed of either fibrous astrocytes or oligodendocytes. Our results indicate that each of these different cortical cell types is generated from a separate population of precursor cells.

Animals↗