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Results for “Astrocyte morphology”

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At least 127 records · Page 7Linked to original sources
PubMed1992

GM1 ganglioside effects on astroglial response in the rat nucleus basalis magnocellularis and its cortical projection areas after electrolytic or ibotenic lesions.

We examined the effects of chronic GM1 ganglioside injections on the astroglial response to bilateral electrolytic or ibotenic acid lesions in the nucleus basalis magnocellularis (NBM) within the NBM and in three cortical projection areas of NBM neurons. Glial fibrillary acidic protein (GFAP) immunohistochemistry was used to visualize the reactive astrocytes. Twenty-six days after injury, extensive astrogliosis was observed within the NBM after both types of lesions. An increased number of GFAP-positive cells were found in the cortex of saline-treated rats following electrolytic but not ibotenic lesions. We suggest that the loss of fibers of passage within the lesion area may account for the difference in cortical gliosis following the two types of damage. Although 17 days of GM1 injections did not affect astrocyte morphology within the NBM, ganglioside treatment reduced the number of GFAP-positive cells after electrolytic but not after ibotenic lesions. Within the cortex, a decrease in GFAP immunoreactivity, size, and number of astrocytes was only observed after electrolytic lesion. These data indicate that a decrease in the astroglial response to injury is the result of an interaction between the type of injury (electrolytic lesion) and chronic GM1 treatment.

Analysis of Variance↗
PubMed1989

Evidence for three morphological classes of astrocyte in the adult rabbit retina: functional and developmental implications.

Commercially available antibodies to glial fibrillary acidic protein (GFAP) and vimentin were used in conjunction with our own antibodies (3F11, MA1 and 4D6) to label astrocytes in the adult albino rabbit retina. Anti-GFAP labels the entire astrocyte population and shows them to be morphologically diverse. By contrast, the remaining four antibodies label different subpopulations of astrocytes. Comparisons of the shapes and distributions of cells composing these subpopulations led us to distinguish three morphological classes: Class A are predominantly perivascular astrocytes, Class B are territorial and rarely contact vessels or axons, Class C (which seems to contain four subclasses) are astrocytes that are predominantly associated with axons.

Animals↗
PubMed2004

The immunohistochemical expression of calcitonin receptor-like receptor (CRLR) in human gliomas.

BACKGROUND: Gliomas are the most common primary tumours of the central nervous system and exhibit rapid growth that is associated with neovascularisation. Adrenomedullin is an important tumour survival factor in human carcinogenesis. It has growth promoting effects on gliomas, and blockade of its actions has been experimentally shown to reduce the growth of glioma tissues and cell lines. There is some evidence that the calcitonin receptor-like receptor (CRLR) mediates the tumorigenic actions of adrenomedullin. AIM: To determine whether CRLR is expressed in human gliomas and the probable cellular targets of adrenomedullin. METHODS: Biopsies from 95 human gliomas of varying grade were processed for immunohistochemical analysis using a previously developed and characterised antibody to CRLR. RESULTS: All tumour specimens were positive for CRLR. As previously found in normal peripheral tissues, CRLR immunostaining was particularly intense in the endothelial cells. This was evident in all the various vascular conformations that were observed, and which are typical of gliomas. In addition, clear immunostaining of tumour cells with astrocyte morphology was observed. These were preferentially localised around vessels. CONCLUSIONS: This study has shown for the first time that the CRLR protein is present in human glioma tissue. The expression of the receptor in endothelial cells and in astrocytic tumour cells is consistent with the evidence that its endogenous ligand, adrenomedullin, may influence glioma growth by means of both direct mitogenic and indirect angiogenic effects. CRLR may be a valuable target for effective therapeutic intervention in these malignant tumours.

Calcitonin Receptor-Like Protein↗
PubMed1997

Live astrocytes visualized by green fluorescent protein in transgenic mice.

Green fluorescent protein (hGFP-S65T) was expressed in transgenic mice under the control of the astrocyte-specific glial fibrillary acidic protein (GFAP) promoter. Tissues from two independent transgenic lines were characterized by Northern blot analysis and by confocal microscopy. The expression pattern in these two lines was identical in all tissues examined, and similar to that found previously with a lacZ transgene driven by the same promoter. Bright fluorescence was observed in the cell bodies and processes of unfixed or fixed astrocytes, using both whole mount and brain slice preparations, from multiple areas of the central nervous system. However, in contrast to GFAP-lacZ transgenics, retinal Müller cells expressed the GFP transgene in response to degeneration of neighboring photoreceptors. These data indicate that the 2.2-kb hGFAP promoter contains sufficient regulatory elements to direct expression in Müller cells, and that GFP is a suitable reporter gene for use in living preparations of the mammalian nervous system. Such mice should prove useful for studies of dynamic changes in astrocyte morphology during development, and in response to physiological and pathological conditions.

Animals↗
PubMed1995

PKA and PKC activation induces opposite glial fibrillary acidic protein (GFAP) expression and morphology changes in a glioblastoma multiform cell line of clonal origin.

Possible differentiation mechanisms were investigated in a glioblastoma multiform cell line (GL15) presenting an undifferentiated phenotype with weak glial fibrillary acidic protein (GFAP) and strong vimentin (VIM) expression. Serum-free conditions induced time-dependent increases of GFAP-mRNA and GFAP protein levels, associated with a process-bearing astrocytic morphology. Activation of protein kinase C (PKC) by tumor promoter phorbol 12-myrystate 13-acetate (PMA) induced a rapid morphological differentiation and a decrease in GFAP mRNA, whereas the GFAP level remained unchanged. Such parameters were shown to characterize a physiological differentiation stage in astroglial cultures. Treatment of process-bearing GL15 cells with dibutyryl cyclic AMP (dbcAMP), a protein kinase A (PKA) activator, induced a time-dependent decrease in the GFAP mRNA and GFAP protein levels and reverted morphological changes induced by serum-free conditions. Neither PMA nor dbcAMP influenced the VIM mRNA expression. In GL15 cells, PKC and PKA activation have opposite effects. Understanding the role of these kinases in malignant transformation and in the in vitro differentiation process is of both basic and clinical interest.

Blotting, Northern↗
PubMed2006

Ammonia-induced alteration in S100B secretion in astrocytes is not reverted by creatine addition.

Hyperammonemia is a major element in the pathogenesis of hepatic encephalopathy (HE) and ammonia neurotoxicity involves an effect on the glutamatergic neurotransmitter system. Astrocytes are intimately related to glutamatergic neurotransmission and, in fact, many specific glial alterations have been reported as a result of ammonia exposure. S100B protein, particularly extracellular S100B, is used as a parameter of glial activation or commitment in several situations of brain injury. However, there is little information about this protein in ammonia toxicity and none about its secretion in astrocytes under ammonia exposure. In this study, we investigated S100B secretion in rat cortical astrocytes acutely exposed to ammonia, as well astrocyte morphology, glial fibrillary acidic protein (GFAP) content and glutamine synthetase (GS) activity. Moreover, we studied a possible effect of creatine on these glial parameters, since this compound has a putative role against ammonia toxicity in cell cultures. We found an increase in S100B secretion by astrocytes exposed to ammonia for 24h, accompanied by a decrease in GFAP content and GS activity. Since elevated and persistent extracellular S100B plays a toxic effect on neural cells, altered extracellular content of S100B induced by ammonia could contribute to the brain impairment observed in HE. Creatine addition did not prevent this increment in S100B secretion, but was able to prevent the decrease in GFAP content and GS activity induced by ammonia exposure.

Ammonia↗
PubMed1996

Targeted deletion in astrocyte intermediate filament (Gfap) alters neuronal physiology.

Glial fibrillary acidic protein (GFAP) is a member of the family of intermediate filament structural proteins and is found predominantly in astrocytes of the central nervous system (CNS). To assess the function of GFAP, we created GFAP-null mice using gene targeting in embryonic stem cells. The GFAP-null mice have normal development and fertility, and show no gross alterations in behavior or CNS morphology. Astrocytes are present in the CNS of the mutant mice, but contain a severely reduced number of intermediate filaments. Since astrocyte processes contact synapses and may modulate synaptic function, we examined whether the GFAP-null mice were altered in long-term potentiation in the CA1 region of the hippocampus. The GFAP-null mice displayed enhanced long-term potentiation of both population spike amplitude and excitatory post-synaptic potential slope compared to control mice. These data suggest that GFAP is important for astrocyte-neuronal interactions, and that astrocyte processes play a vital role in modulating synaptic efficacy in the CNS. These mice therefore represent a direct demonstration that a primary defect in astrocytes influences neuronal physiology.

Animals↗
PubMed2006

Amyloid precursor protein is involved in staurosporine induced glial differentiation of neural progenitor cells.

Staurosporine (STS) has been reported as not only a pro-apoptotic agent, but also a terminal differentiation inducer in several neuroblastoma cell lines. Here, we report involvement of amyloid precursor protein (APP) in a STS induced astrocytic differentiation of human neural progenitor cells (NT-2/D1). We found that STS-treated NT-2/D1 cells expressed astrocyte-specific glial fibrillary acidic protein (GFAP), aspartate transporter, and glutamate transporter-1 with a distinctive astrocytic morphology. STS treatment increased GFAP promoter activity and increased expression and secretion of APP in NT-2/D1 cell culture. Overexpressed APP enhanced GFAP promoter activity and expression of GFAP, while gene silencing of APP by RNA interference decreased GFAP expression. These results indicate involvement of APP in STS induced astrocytic differentiation of NT-2/D1 cells. Furthermore, suppression of ERK1/2 phosphorylation, which is known to regulate APP expression by a MEK1 inhibitor, PD098059, reduced both APP and GFAP expression in STS treated NT-2/D1 cells. Thus, STS may induce astrocytic differentiation of NT-2/D1 by increasing APP levels associate with activation of ERK pathway.

Amyloid beta-Protein Precursor↗
PubMed1998

Microglial/macrophage accumulation during cuprizone-induced demyelination in C57BL/6 mice.

To study microglial/macrophage infiltration, a cuprizone-induced model for demyelination in C57BL/6 mice was established. Cuprizone is known to cause demyelination in Swiss mice, however, cuprizone-induced demyelination in C57BL/6 mice has not been previously described. Induction of demyelination in C57BL/6 mice enables examination of the function of microglia/macrophage through comparative analyses of syngeneic mice with various targeted genetic mutations. In this report, cuprizone-induced demyelination is easily inducible, localized, and predictable. Concurrent with the initiation of demyelination, we noted microglial/macrophage accumulation and changes in astrocyte morphology. Astrogliosis promptly followed microglia/macrophage recruitment. These observations suggested that microglia/macrophage actively contribute to the demyelination process.

Animals↗
PubMed1999

Regenerative potential of adult O1+ oligodendrocytes.

Remyelination in the adult central nervous system (CNS) is preceded by the generation of new oligodendrocytes (ODCs) but the source of the new ODCs has not been resolved. Adult galactocerebroside positive (O1+)ODCs proliferate when cultured with purified sensory neurons (Wood and Bunge, Nature 320:756-758, 1999), implying that differentiated ODCs could be an important source of new myelinating ODCs. To test this possibility purified O1+ODCs (>96% purity) were plated at low density (20-50 cells/culture) into cultures of purified dorsal root ganglion neurons. Three days after plating, single O1+ODCs were located (209 ODCs/43 cultures) and sequentially observed for 4 weeks. The ODCs began to proliferate by the fifth day after plating and formed large colonies by the third week. Most cells in these colonies were 01- but positive for another ODC antigen, O4. A few O1+, myelin basic protein (MBP)+ODCs, and glial fibrillary acidic protein (GFAP)+cells with astrocytic morphology were observed in some colonies. In similar cultures plated with cell-sorted O1+ODCs (>99.5% purity), ciliary neurotrophic factor (CNTF, 1ng/ml) increased the number and size of colonies, the number of O1+MBP+ODCs (including ODCs producing myelin-like profiles in association with axons) and the number of GFAP+ astrocytes, relative to untreated controls. The results are evidence that CNTF exerts a trophic effect on adult O1+ODCs, and/or their progeny, and that cells generated by division of O1+ODCs can become either new myelin-producing ODC, or astrocytes. This plasticity in regenerative potential of adult O1+ODCs has not been previously demonstrated.

Animals↗
PubMed2003

Oxidative stress induces axonal beading in cultured human brain tissue.

Oxidative stress has been implicated in the pathogenesis of a number of human neurodegenerative disorders of the central nervous system (CNS), including Alzheimer's disease (AD). To better understand the pathological effects of oxidative stress on CNS neurons we used a primary human brain cell culture model of hydrogen peroxide-induced oxidative stress. Neuronal and astrocytic morphology was visualised by immunofluorescence with antibodies to the neuron-specific microtubule component beta-tubulin III and against glial fibrillary acidic protein (GFAP), respectively. After exposure to 40 mM H(2)O(2) for 60-90 min, axonal swelling was observed, which developed into axonal beading after 48 h. No beading was observed in GFAP-positive astrocytes. Despite the concentration of H(2)O(2) used, neurons remained attached to the substratum and showed no signs of apoptosis. This was attributed to the neuroprotective effect of the B-27 medium supplement, which contained antioxidants. The axonal swelling and beading was consistent with a disruption of microtubules by oxidative stress and subsequent hold-up of axonal transport.

Antioxidants↗
PubMed2003

Calpain 3 is expressed in astrocytes of rat and Microcebus brain.

The calcium-dependent protease calpain is involved in numerous functions, including the control of cell survival, plasticity and motility. Whereas the isoforms calpain 1 and 2 have been described as ubiquitously expressed enzymes, calpain 3 has been called "muscle-specific", although trace amounts of calpain 3 mRNA have been detected by Northern blot in brain homogenates. In this study, we validated antibodies raised either against the peptides that were specific for a given isoform or the peptides present in all the three isoforms. We then used the anti-calpain 3 antibodies together with antibodies directed against cell-type-specific proteins to determine by double- and triple-labelling immunocytochemistry if the protease is expressed in specific cell populations of rat as well as lesser mouse lemur (Microcebus murinus) brain. Calpain 3 was almost exclusively found in cells displaying astrocyte morphology. These cells, most of which co-expressed glial fibrillary acidic protein, were particularly numerous close to the striatal subventricular zone (where numerous neurones forming the rostral migratory stream (RMS) towards the olfactory bulbs are generated) and the RMS itself. Other immunoreactive cells were found close to the pial surface of the forebrain, in the corpus callosum and in the dentate gyrus. Calpain 3 may be involved in astrocyte plasticity and/or motility.

Animals↗
PubMed1999

Neuroaxonal pathology in Creutzfeldt-Jakob disease.

Neuroaxonal pathology has met little attention in transmissible spongiform encephalopathies. In brains of a series of 39 consecutive Creutzfeldt-Jakob disease (CJD) cases, we detected numerous abnormal neurites that labeled for neurofilament proteins (NFP) by immunocytochemistry. Three types of abnormally NFP-accumulating structures were more prominently observed in CJD brains than in age-matched control brains: 1. Neurons with NFP in their somata were seen in 29 CJD cases (74%), some appearing distended with eccentrically placed nuclei and homogenously stained cytoplasm. 2. Neuritic distensions (neuritic swellings, dystrophic neurites) were observed mainly in the white matter but also at the junction between gray and white matter. In some axons many such swellings could be traced along the visible part of the axonal segment. 3. Axonal spheroids were observed mainly in the medulla, predominantly but not exclusively in posterior nuclei, and were more numerous than in age-matched control brains. Several neurons, axons and spheroids demonstrated immunoreactivity for amyloid precursor protein. Their number was much smaller, however, than that of NFP-immunoreactive structures and varied from one or two immunopositive neurites per section to small clusters of beaded or spiral axons. Focal expression of apolipoprotein E in cells of microglial and astrocytic morphology was observed in areas with most pronounced axonal damage. We conclude that neuroaxonal pathology is a frequent and important part of brain lesioning in CJD, probably reflecting profound impairment of axonal transport.

Adult↗
PubMed1999

Overexpression of nerve growth factor and basic fibroblast growth factor in AIDS dementia complex.

Although neurotrophic factors are currently considered as treatment for neurodegenerative diseases, little is still known about their presence in the central nervous system under pathological conditions. We investigated the expression of the neurotrophic molecules NGF, bFGF, BDNF and IGF-1 in brain tissue of patients suffering from AIDS dementia complex. In contrast to IGF-1 and BDNF, NGF and bFGF mRNA levels were significantly elevated. Strong NGF immunoreactivity was found in perivascular areas and was colocalized with infiltrating macrophages, whereas intense bFGF staining was found in cells with characteristic astrocytic morphology. These data suggest that the induction of NGF and bFGF alone appears to be insufficient as a compensatory mechanism to prevent ADC.

AIDS Dementia Complex↗
PubMedDate not supplied

Myelin staining of archival brain tissue.

To evaluate the feasibility of staining for myelin in archival materials, paraffin blocks were prepared from brain tissue that had been in formalin for intervals ranging from 7 months to over 53 years. Verhoeff and Luxol fast blue stains of the resulting sections yielded staining whose quality was unaffected by duration of fixation. Myelinated and unmyelinated areas were clearly distinguished, and the morphology of individual myelin sheaths was well-preserved. No changes to conventional protocols were required, but it was necessary carefully to monitor the progress of differentiation. With antigen retrieval, it was possible to display immunoreactivity for myelin basic protein. While this persisted even after prolonged fixation, fine detail was lost from the myelin sheaths, and there was staining of oligodendroglial cytoplasm and nuclei, which was not seen in recently fixed tissue. In contrast to this loss of detail in myelin sheaths, immunohistochemistry for glial fibrillary acidic protein displayed astrocytic morphology clearly, even in the oldest tissue. We conclude that archival, formalin-fixed material can be adequately examined for myelin loss and astrocytosis.

Adult↗
PubMed2005

The differential response of astrocytes within the vestibular and cochlear nuclei following unilateral labyrinthectomy or vestibular afferent activity blockade by transtympanic tetrodotoxin injection in the rat.

In this study, we investigated whether changes in the vestibular neuronal activity per se influence the pattern of astrocytes morphology, glial fibrillary acidic protein (GFAP) expression and ultimately their activation within the vestibular nuclei after unilateral transtympanic tetrodotoxin (TTX) injections and after unilateral inner ear lesion. The rationale was that, theoretically the noninvasive pharmacological functional blockade of peripheral vestibular inputs with TTX, allowed us to dissociate the signals exclusively related to the shutdown of the resting activity of the first-order vestibular neurons and from neuronal signals associated with trans-ganglionic changes in first order vestibular neurons induced by unilateral labyrinthectomy (UL). Since the cochlea was removed during the surgical procedure, we also studied the astrocytic reaction within the deafferented cochlear nuclei. No significant changes in the distribution or relative levels of GFAP mRNA expression, relative levels of GFAP protein or immunoreactivity for GFAP were found in the ipsilateral vestibular nuclei at any post-TTX injection times studied. In addition, no sign of microglia activation was observed. In contrast, a robust increase of the distribution and relative levels of GFAP mRNA expression, protein levels and immunoreactivity was observed in the deafferented vestibular and cochlear nuclei beginning at 1 day after inner ear lesion. GFAP mRNA expression and immunoreactivity in the cochlear nucleus was qualitatively stronger than in the ipsilateral vestibular nuclei. The results suggest that astrocyte activation in the vestibular nuclei is not related to drastic changes of vestibular nuclei neuronal activity per se. Early trans-ganglionic changes due to vestibular nerve dendrites lesion provoked by the mechanical destruction of vestibular receptors, most probably induced the glial reaction. Its functional role in the vestibular compensation process remains to be elucidated.

Afferent Pathways↗
PubMed1997

Quantification of the effects of astrocytes on oligodendroglial morphology.

Oligodendrocytes in neonatal rat forebrain cultures grow either in isolation of other cells or upon astrocytes. Populations of both types of oligodendrocytes were used to quantify the effects of astrocytes on oligodendroglial morphology. Changes in oligodendroglial size and shape were determined by measurement of total process length, cell area, growth area, and fractal dimension. The directionality of process growth, quantified by measurement of the axes of growth, was also compared. Isolated oligodendrocytes exhibited greater total process length, greater cellular area, larger growth area, and a more complex boundary than oligodendrocytes growing upon astrocytes. Analysis of the axes of cellular growth revealed that the processes of isolated oligodendrocytes exhibited radial symmetry, whereas the processes of oligodendrocytes growing upon astrocytes were limited to an area demarcated by the astrocytic processes. These data suggest that, in neuron-free culture, the growth of oligodendroglial processes is modified by underlying astrocytic processes.

Animals↗
PubMedDate not supplied

Alterations induced by lithium in gfap expression and in the proteinic composition of glial cells in vitro.

In the adult brain, astrocytes account for about 40% of the cell population in the central nervous system. Normal, reactive and neoplastic astrocytes can be identified in immunohistochemical preparations by means of glial fibrillary acid proteins (GFAP) expression. This protein is considered to be a sensitive indicator of xenobiotics toxicity. Previous studies have demonstrated that 2 mM LiCl induce alterations of astrocyte morphology after 18-20 days of treatment in vitro. We have decided to study GFAP expression under such conditions. Immunodetection and Western blotting assays have shown 2 mM of LiCl to induce alterations of GFAP expression both after 12 days of treatment and after 18-20 days. Moreover, 2 mM of LiCl induce an alteration of the proteinic composition of cells.

Animals↗