Membrane structure in cultured astrocytes

Landis, Dennis M.D.; Weinstein, Lori A.

doi:10.1016/0006-8993(83)90545-0

Cited by 30 publications

(13 citation statements)

References 34 publications

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“…Interestingly, we found numerous tight junctions and desmosomes between astrocytes in close proximity to endothelial cells (Fig. 8C); such membrane specializations have not been described so far between mammalian astrocytes (Landis & Weinstein, 1983) but they are known to constitute the blood–brain barrier in lower animals (Abbott & Bundgaard, 1992). Tight junctions were also present between endothelial cells, and they were visibly more abundant than in monocultures of endothelial cells, as has been demonstrated in other coculture models (Janzer & Raff, 1987; Nagy & Martinez, 1991).…”

Section: Resultssupporting

confidence: 73%

Astrocyte–endothelial cell calcium signals conveyed by two signalling pathways

Braet

Paemeleire

D’Herde

et al. 2001

Eur J of Neuroscience

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Astrocytes and endothelial cells are in close contact with each other at the blood-brain barrier, where important molecular transports take place. Despite these key morphological and functional properties, little is known regarding the dynamic signalling processes that occur between these two cell types. We investigated astrocyte-endothelial cell calcium signalling mechanisms in a coculture model prepared from primary rat cortical astrocytes and ECV304 cells. We used flash photolysis of caged inositol-trisphosphate (IP3) and gentle mechanical stimulation to trigger astrocyte-endothelial cell calcium signals and to investigate the underlying propagation mechanisms. Photolytically releasing IP3 in a single cell triggered increases in cytoplasmic calcium concentration that propagated between astrocytes and endothelial cells in either direction. These propagating calcium signals did not cross cell-free zones and were not affected by fast superfusion or by the purinergic inhibitors apyrase and suramin, indicating that they are communicated through an intracellular pathway in conjunction with gap junctions. Electrophysiological experiments confirmed a low degree of astrocyte-endothelial cell electrical cell-to-cell coupling. Mechanical stimulation of a single cell also triggered astrocyte-endothelial cell calcium signals but, in contrast to the former triggering mode, these signals crossed cell-free zones and were significantly inhibited by apyrase, thus indicating the involvement of an extracellular and purinergic messenger. Astrocyte-endothelial cell calcium signalling also occurred in cocultures prepared with astrocytes and primary rat brain capillary endothelial cells. We conclude that astrocytes and endothelial cells can exchange fast-acting calcium signals (time scale of seconds) that can be communicated through an intracellular/gap junctional pathway and an extracellular purinergic pathway.

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Section: Resultssupporting

confidence: 73%

Astrocyte–endothelial cell calcium signals conveyed by two signalling pathways

Braet

Paemeleire

D’Herde

et al. 2001

Eur J of Neuroscience

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“…E17 hippocampal neuronal cultures were isolated according to the method of Banker (1980) with some modifications (Abele et al, 1990;Scholz and Miller, 1991) and grown on coverslips. Rat cortical astrocytes were cultured following the method of Landis and Weinstein (1983). The astrocytes were used for virus infection when they had reached confluency in DM EM with 5% horse serum and maintained in DM EM with N2.1 in the presence of AraC to prevent cell proliferation.…”

Section: Methodsmentioning

confidence: 99%

Mutant Superoxide Dismutase-1-Linked Familial Amyotrophic Lateral Sclerosis: Molecular Mechanisms of Neuronal Death and Protection

Ghadge¹,

et al. 1997

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Mutations in human Cu/Zn superoxide dismutase-1 (SOD) cause ϳ20% of cases of familial amyotrophic lateral sclerosis (FALS). We investigated the mechanism of mutant SODinduced neuronal degeneration by expressing wild-type and mutant SODs in neuronal cells by means of infection with replication-deficient recombinant adenoviruses. Expression of two FALS-related mutant SODs (A4V and V148G) caused death of differentiated PC12 cells, superior cervical ganglion neurons, and hippocampal pyramidal neurons. Cell death included many features typical of apoptosis. Death could be prevented by copper (Cu 2ϩ ) chelators, Bcl-2, glutathione, vitamin E, and inhibitors of caspases. Mutant SOD-expressing PC12 cells had higher rates of superoxide (O 2 Ϫ ) production under a variety of conditions. The results support the hypothesis that mutant SOD induced-neurodegeneration is associated with disturbances of neuronal free radical homeostasis.

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“…The data were presented as singleaccording to the method of Landis and Weinstein (1983). Cerebral Figure I.…”

Section: Motoneuronsmentioning

confidence: 99%

Fluorescence-activated cell sorting of embryonic mouse and rat motoneurons and their long-term survival in vitro

1987

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Motoneurons from embryonic mice and rats were labeled with retrogradely transported succinyl wheat germ agglutinin (WGA)-fluorescein isothiocyanate (FITC). After dissociation of the spinal cord, fluorescent motoneurons were isolated by flow cytometry. Sorted motoneurons were maintained for as long as 6 weeks in vitro on monolayers of astrocytes in muscle-conditioned medium. Immunocytochemical staining of the cultures for various neuronal antigens suggested that sorted motoneurons are receptive to GABAergic and glycinergic, as well as cholinergic, innervation. Many of the sorted cells were also labeled intracellularly with antibodies to choline acetyltransferase (ChAT) and GABA.

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Membrane structure in cultured astrocytes

Cited by 30 publications

References 34 publications

Astrocyte–endothelial cell calcium signals conveyed by two signalling pathways

Astrocyte–endothelial cell calcium signals conveyed by two signalling pathways

Mutant Superoxide Dismutase-1-Linked Familial Amyotrophic Lateral Sclerosis: Molecular Mechanisms of Neuronal Death and Protection

Fluorescence-activated cell sorting of embryonic mouse and rat motoneurons and their long-term survival in vitro

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