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Results for “Astrocyte morphology”

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At least 19 recordsLinked to original sources
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↗
PubMed1991

Effects of sphingosine on phorbol ester-mediated changes in astrocyte morphology and protein phosphorylation.

Previous studies indicate that phorbol myristate acetate (PMA) can induce morphological changes in astrocytes cultured from the rat neocortex. PMA also increased 32P incorporation into several proteins, including glial fibrillary acidic protein (GFAP), vimentin, and proteins with molecular weights of 80,000 (pI 4.5), 50,000 (pI 4.9), and 30,000 (pI 5.5). The present studies were conducted to determine if the morphological effect and the phosphorylation effect of PMA could be blocked by treatment with sphingosine, a protein kinase C inhibitor. Treatment with 15 microM sphingosine inhibited the effect of PMA on astrocyte morphology. This agent also inhibited the increase in phosphorylation mediated by PMA. The percent inhibition ranged from approximately 20% for the 30,000-Mr protein to 70% for GFAP. Analysis of phosphorylation sites on GFAP and vimentin using two-dimensional tryptic mapping techniques indicate that the partial inhibition of phosphorylation is likely the consequence of partial inhibition of protein kinase C rather than a selective inhibition at some phosphorylation sites and not others. In addition to increasing 32P incorporation into various proteins, PMA also decreased 32P incorporation in several 20,000-Mr proteins (pI values of 6.7, 6.4, 6.2, 4.9). However, this effect was not blocked by treatment with sphingosine. This suggests that the actions of PMA to increase and decrease 32P incorporation are mediated by different mechanisms.

Animals↗
PubMed1990

Phorbol ester-induced change in astrocyte morphology: correlation with protein kinase C activation and protein phosphorylation.

Treatment with 300 nM phorbol 12-myristate 13-acetate (PMA) transforms polygonal-shaped cultured astrocytes into process-bearing cells and produces a shift in protein kinase C (PK-C) from the cytosol to the membrane. Exposure to PMA also produces increases in the phosphorylation of several proteins including vimentin, glial fibrillary acidic protein (GFAP), an acidic 80,000 molecular weight protein, and two 30,000 molecular weight proteins (pI 5.5 and 5.7). The effects of PMA on the translocation of PK-C and on protein phosphorylation precede the PMA-induced changes in astrocyte morphology, and a close correlation exists between the concentration of PMA necessary to elicit half-maximal and maximal effects on the shift of PK-C to the membrane and on protein phosphorylation. In addition, the PMA-induced alterations in cell morphology are not permanent, and within 24 hr after PMA treatment the cells have reverted almost to their original morphology. A second exposure to PMA at this time fails to elicit further change in cell shape and is also incapable of producing increases in the phosphorylation of proteins. It was determined that there is little, if any, PK-C present in these PMA-pretreated cells. The morphological responsiveness to PMA gradually returns in 5 to 8 days after the initial treatment with PMA, and this is accompanied by the recovery of PK-C activity and the phosphorylation response. Therefore, these studies suggest that the effect of PMA on astrocyte morphology is mediated by the activation of PK-C and subsequent protein phosphorylation.

Animals↗
PubMed1989

Astrocyte morphology altered by 1-(5-isoquinolinylsulfonyl) 2-methyl piperazine (H-7) and other protein kinase inhibitors.

Studies were conducted to determine if the protein kinase C inhibitor H-7 could block the effects of phorbol-12-myristate-13-acetate (PMA) on astrocyte morphology. Contrary to expectation, H-7 alone was found to induce morphological changes very similar to those elicited by PMA. This effect was shared by two other inhibitors of protein kinase C, H-8 and staurosporine, but not by the cyclic nucleotide-dependent protein kinase inhibitor HA-1004 or the calcium/calmodulin dependent protein kinase inhibitor W-7. Although the morphological effects observed with H-7 resemble those induced by PMA, H-7 did not promote the redistribution of protein kinase C to the membrane or induce the phosphorylation of endogenous proteins like PMA. In addition, the effects of H-7 were still observed in cells depleted of protein kinase C activity which were no longer responsive to treatment with PMA. Cytoskeletal elements appear to be involved in the effect of H-7 on cell shape since this effect is blocked by treatment with colchicine. Activators of the cyclic AMP-dependent protein kinase also alter astrocyte shape, however, while H-7 did cause a slight increase in cyclic AMP levels, it was unlikely that this action is responsible for its effect on morphology. One common action of both H-7 and PMA was to decrease the 32P content of several 20,000 Da proteins. While the mechanism by which H-7 exerts its influence on astrocyte morphology remains to be clarified, be it by the inhibition of protein kinase C or some other mechanism, the results suggest that caution must be used when interpreting the effects of activators and inhibitors of this kinase.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1990

Reversibility of ganglioside effects on astrocyte morphology.

The B-subunit of cholera toxin (BCT) induces a morphological change in cultured rat cerebral astrocytes from flat (epithelioid) to stellate (process-bearing). This stellation is reversed by the gangliosides GM1 and GD1a at concentrations of 10 microM or higher. Upon changing to a ganglioside-free medium, the flat astrocytes reacquire the stellate morphology within 3 hr, indicating that the antistellation effect of gangliosides is reversible. The possibility that this reversibility was due to a loss of exogenously acquired gangliosides from the cell membrane can be ruled out since pretreatment with GM1, but not GD1a, which does not bind BCT, results in an increased responsiveness to BCT, which was identical whether measured immediately after withdrawal of the ganglioside or 3 hr later. Asialo-GM1, which neither binds BCT nor reverses BCT-induced stellation by itself, prevents the return to stellation after withdrawal of the gangliosides. These data suggest that while gangliosides remain associated with the cell, their effect on astrocytes can change from opposing to permitting the stellate morphology.

Animals↗
PubMed1986

Comparison of astrocytic morphology, proliferation, marker profile and response to neurons in wild-type and weaver mutant mouse cerebella in culture.

In serum-free monolayer cultures of early postnatal weaver (wv/wv) cerebellum granule neurons show decreased attachment, survival and neurite outgrowth when compared to wild-type (+/+) littermate cultures. wv/wv Astrocytes display a more epithelioid morphology and altered proliferation. However, both morphology and proliferation of wv/wv astrocytes were reversed to a normal phenotype by addition of purified small neurons from early postnatal cerebella from +/+ animals. Attachment of +/+ neurons to wv/wv astrocytes was not significantly different from that of +/+ astrocytes and antigenic marker profiles of wv/wv and +/+ astrocytes differed only slightly. Attempts failed to revert the abnormal wv/wv phenotype in neurons by addition of gangliosides, triiodothyronine T3, prostaglandin A2, medium containing 1% horse serum, conditioned medium from +/+ cerebellar cultures, or by cocultivation with +/+ astrocytes. We would like to suggest that the primary defect of the wv/wv mutation is predominantly an abnormality in granule cell neurons, but not of the vast majority of astrocytes.

Animals↗
PubMed2026

Astrocyte reactivity by alcohol dependence in the central amygdala.

Astrocytes play essential roles in maintaining brain homeostasis and in contributing to synaptic functions, but, in response to injury, infection, or disease, astrocytes can downregulate their homeostatic and physiological functions while increasing neuroinflammatory responses. The central amygdala (CeA) is important for stress responsivity and the development of alcohol (ethanol) dependence. Using a multi-omics approach in Aldh1l1-EGFP/Rpl10a mice and the chronic intermittent ethanol two-bottle choice (CIE-2BC) model, we have characterized the translational response of CeA astrocytes, as well as the proteomic and phosphoproteomic changes in ethanol dependent, non-dependent, and naïve mice. We identified astrocyte-specific alterations in neuroimmune functions and antioxidant/oxidative stress pathways in ethanol dependent mice as well as cytoskeletal plasticity related pathways in non-dependent mice. Proteomic analysis showed down-regulation of astrocyte physiological functions in dependent animals while phosphoproteomic analysis identified pathways associated with cytoskeleton remodeling in both dependent and non-dependent mice. Reconstructions of astrocyte morphologies demonstrated increased CeA astrocyte complexity in dependent and non-dependent groups compared to naïve mice. The astrocyte-specific activation of neuroimmune and antioxidant pathways, down-regulation of homeostatic functions, alteration in protein phosphorylation-mediated cytoskeleton remodeling, and increased astrocyte morphological complexity demonstrate that ethanol dependence induces astrocyte reactivity in the CeA consistent with both adaptive and maladaptive changes. These findings highlight the role of CeA astrocytes in the progression from alcohol intake to dependence and represent a first step toward identifying astrocyte-specific therapeutic strategies to treat Alcohol Use Disorder (AUD) aimed at potentiating reactive astrocyte adaptive changes and inhibiting maladaptive responses.

Animals↗
PubMed1987

Synergistic action of thyroid hormone, insulin and hydrocortisone on astrocyte differentiation.

We report here on the synergistic regulation of astrocyte development by 3 hormones: thyroid hormone (TH), insulin, and hydrocortisone (HC). Their effect, in a defined serum-free media, on astrocyte morphology, on glia fibrillary acidic protein (GFAP) immunostaining pattern, and on glutamine synthetase (GS) was investigated. TH transformed the flat, polygonal astrocytes into process-bearing cells. This effect was accentuated by insulin, which by itself had no effect on astrocyte morphology. The morphological transformations were accompanied by changes in the pattern of GFAP immunostaining which indicated a more organized and directed cytoskeleton arrangement in the TH-insulin treated cultures. Over 95% of the cells in the culture expressed GFAP. All 3 hormones regulated GS levels. TH increased GS levels by 50% and insulin raised its levels by 3-fold. While having no effect on astrocyte morphology, HC increased GS levels by 3.7-fold in both the hormone-free and insulin-supplemented medium. HC acted synergistically with insulin in its action on GS bringing about a 12-fold increase in the enzyme activity. In contrast, TH did not interact with insulin and was additive with HC in its action on GS. The continuous presence of insulin and TH was required to maintain their morphological and GS effect, suggesting that these hormones might not only be important for astrocyte differentiation, but later on for astrocyte function as well. Since astrocytes interact with and affect neurons and oligodendrocytes, the findings reported here might have bearing on the development and function of these other brain cells as well.

Animals↗
PubMed1985

Localization of immunoglobulins G, A and M in glial cells of reactive and neoplastic origin.

The localization of immunoglobulins G, A and M in glial cells of neoplastic and reactive origin have been investigated by the use of the PAP (peroxidase-antiperoxidase) method on paraffin embedded tissue previously fixed in calcium formol. It has been found, that some glial cells of astrocyte type showed a very intense staining when oligoclonal antibodies to human immunoglobulins G, A and M specific for gamma, alpha, and mu chains were used. The localization of immunoglobulins was disclosed in astrocytes of various morphology; astrocytes with well developed processes, gemistocyte type cells without or only with short and thick cell processes and in small cells with scanty cytoplasm. The number of cells with immunoglobulins localized is very small. No positive results have been noted if the normal brain tissue is concerned. The specificity of the method is discussed.

Astrocytes↗
PubMed1988

Phorbol ester and dibutyryl cyclic AMP reduce content and efflux of taurine in primary cerebellar astrocytes in culture.

In 16-18 days in vitro (DIV) primary astrocyte cultures prepared from 7- to 9-day-old rats, 48 h exposure to 12,13-phorbol dibutyrate (PDBU) (1 microM) or dibutyryl cAMP (dbcAMP) (1 mM) reduced cellular taurine content, and both basal and 50 mM K+-evoked taurine efflux, but did not alter cellular glutamate or total protein content. Decreases in cellular taurine content first became apparent between 1 and 6 h and were maximal after 24 h. Treatment also rapidly altered astrocyte morphology to a more process-bearing form within 1 h. In contrast, fibroblast growth factor (FGF), epidermal growth factor (EGF), dbcGMP and alpha-PDBU did not affect cellular morphology, amino acid content or taurine efflux at any time tested. These findings suggest that, while protein kinase C translocation and adenylate cyclase activation may be only indirectly involved in the regulation of astrocyte morphology, long-term decreases in cellular taurine content and efflux may be the more direct result of these second messenger systems.

Animals↗
PubMed1992

Ultrastructural characterization of transitional cells in oligodendrogliomas.

In oligodendroglial tumors the expression of glial fibrillary acidic protein (GFAP) is found in cells with an astrocytic morphology representing preexistent or neoplastic astrocytes. In addition, a proportion of the GFAP-positive cells has the morphology of miniature gemistocytes (minigemistocytes) or oligodendrocytes (gliofibrillary oligodendrocytes or GFOC). Both minigemistocytes and GFOC are considered as cells transitional between astrocytic and oligodendroglial lineage. Though minigemistocytes can readily be distinguished in routinely stained histological sections, GFAP immunostaining is obligatory for the identification of the GFOC. In the present study, the GFOC is characterized at the ultrastructural level using an immunogold-silver stain on semithin (1 micron) slides for identification of GFAP immunoreactivity and subsequent processing of the adjacent slide for immunoelectron microscopy. In analogy with the minigemistocytes, the glial filaments in the GFOC are arranged in parallel bundles. The finding of cells with ultrastructural features intermediate between those of GFOC and minigemistocytes suggests a close relationship and a possible interconvertibility between the two transitional cell types in oligodendrogliomas.

Adult↗
PubMed1987

Morphological changes in cultured astrocytes following exposure to calcium ionophores.

Induced differentiation of cultured astrocytes to a process-bearing morphology has been described with a variety of agents known to increase intracellular cyclic AMP. The ionophores A23187 and ionomycin were found to induce a reversible change in astrocyte morphology to a process-bearing form. Cell death also occurs following exposure to either A23187 or ionomycin. This change in morphology which occurs following exposure to ionomycin in calcium- and serum-containing Dulbecco's Modified Eagle's medium also occurs in the absence of extracellular calcium. These findings suggest a role for other second messengers than cyclic AMP in controlling astrocyte morphology.

Animals↗
PubMed1992

[Regulation by chloride ion of astroglial cell functions and morphological transformation].

Recently, several lines of evidence have indicated the important roles of glial cells, especially astrocytes, in the regulation of neuronal functions. The neuron-glia interaction is one of the most important issues in neuroscience, including neuropharmacology. I reviewed the present status and perspectives on the physiologic and pathologic functions of astrocytes in relation to the roles of intracellular Cl-. Astrocytes have different types of Cl- transport systems, such as voltage-sensitive and ligand-gated channels; HCO3(-)-Cl- exchange; and Na+, K+, Cl- cotransport systems. Anion exchange and cotransport systems are responsible for intracellular pH regulation and astrocytic volume regulation, respectively. Especially, astrocytic volume regulation is physiologically important for reducing the concentrations of K+ and glutamate in the extracellular space by their uptake systems. Disturbance of astrocytic volume regulation is expressed as astrocytic swelling, which is usually observed in various brain pathologic states including ischemia. Experimentally, glutamate caused a typical swelling of astrocytes in culture by Cl- and Ca(++)-dependent processes. Glutamate-induced swelling is qualitatively different from reversible swelling induced by hypoosmotic medium. Recently, we found that Cl- is intracellular factor for modulating the receptor-adenylate cyclase system in brain slices. Similarly, the receptor- and forskolin-stimulated adenylate cyclase of astrocytes showed a clear Cl- dependence. This was functionally confirmed by astrocytic morphological transformation induced by the cyclic AMP system.

Astrocytes↗
PubMed1988

Reactive astrocytes in the morphologic composition of peripheral areas of gliomas.

The participation of reactive astrocytes in the morphologic composition of peripheral areas of 25 gliomas was investigated. Reactive astrocytes were studied by the immunohistochemical demonstration of glial fibrillary acidic protein and vimentin. Reactive astrocytes were more abundant around malignant gliomas than around well-differentiated astrocytomas. They underwent modifications when entrapped within the tumor proliferation and became indistinguishable from tumor astrocytes. Mitoses occurred in both types of cells. Reactive astrocytes did participate in the cell composition of gliomas. They might have contributed to tumor growth. Practically, their occurrence might lead to an erroneous diagnosis when small fragments of tissue are examined.

Astrocytes↗
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↗