Glial Cells and Amino Acid Transmitters

Hamberger, Anders; Sellström, Åke; Weiler, C.T.

doi:10.1007/978-1-4613-4030-0_46

Cited by 5 publications

(2 citation statements)

References 24 publications

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“…It is conceivable, although highly conjectural, that oligodendrocytes specialize in their response to neurotransmitters depending on their location within the nervous tissue and relative to particular neuronal cell types and their particular neurotransmitter as it has been suggeted for astrocytes (Hamberger et al, 1977). Whether our culture system indeed reflects the cellular properties of oligodendrocytes in uiuo remains an open question.…”

Section: Discussionmentioning

confidence: 96%

gamma-Aminobutyric acid directly depolarizes cultured oligodendrocytes

1984

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gamma-Aminobutyric acid (GABA) depolarizes in a dose-dependent manner approximately one-third of all immunologically identified oligodendrocytes in cultures of mouse spinal cord. Measurements of [K+]o indicate that the response to GABA is not due to K+ released from active neurons. The depolarization is not accompanied by a change in cell input resistance. Replacement of sodium in the bathing solution abolishes the entire response, whereas ouabain only inhibits the repolarization phase. Current clamp experiments with two separate intracellular electrodes show that the depolarization increases at more positive potentials while the repolarization increases at more negative potentials. Bicuculline and picrotoxin but not nipecotic acid reduce the GABA effect. Pentobarbital and chlordiazepoxid also reduce the GABA-induced depolarization. Muscimol produces a depolarization similar to that of GABA. Heterogeneity in the oligodendrocyte population is indicated by the observation that some cells respond to both GABA and glutamate, while others respond only to one and some are not responsive to either.

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Section: Discussionmentioning

confidence: 96%

gamma-Aminobutyric acid directly depolarizes cultured oligodendrocytes

1984

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“…It is likely that not only the fine details of culture conditions play an Astrocytes support incomplete differentiation of an oligodendrocyte precursor cell important role, but that the developmental committment of the two glial precursor cells with the same marker phenotype is different. The signals which lead to a divergent deployment of glia might be due to different cellular and molecular environments as have been suggested to exist for differentiated astrocytes which differ from one brain region to another in their response to neurotransmitters (Hamberger et al, 1977), in their influence on neuronal morphology (Denis-Donini et al, 1983) and in biochemical composition (Raff et al, 1983a;Schachner, 1982). By use of cell type-and stage-specific markers and highly enriched neural cell populations the decisive signals that lead to complete differentiation of an oligodendrocyte from a precursor cell is open to analysis in vitro.…”

mentioning

confidence: 99%

Astrocytes support incomplete differentiation of an oligodendrocyte precursor cell.

Keilhauer¹,

Meier²,

Kuhlmann-Krieg³

et al. 1985

The EMBO Journal

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Glial fibrillary acidic protein‐positive astrocytes, but not neurons or fibroblasts, support the differentiation of an oligodendroglial precursor cell expressing O4 antigen and vimentin into an O4 antigen‐positive, but vimentin‐negative oligodendrocyte. Further maturation into galactocerebroside (O1)‐positive oligodendrocytes is, however, not achieved under the culture conditions used, neither in the presence of astrocytes nor neurons.

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Glutamate‐induced cellular injury in isolated chick embryo retina: Müller cell localization of initial effects

Casper

Trelstad

Reif‐Lehrer

1982

J of Comparative Neurology

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The neurotoxic and gliotoxic effects of glutamate and several glutamate analogues were studied in isolated chick embryo retinas. To facilitate examination of initial pathological events, a short-term incubation system was developed and used for light microscopic and autoradiographic investigation. Low-dose, short-term glutamate treatment of 12-day retinas resulted in a glial-specific lesion in the Müller cells, characterized by extensive cellular edema; at higher concentrations and/or longer treatment times, neurotoxic as well as gliotoxic effects were seen. The early glial damage was identical in appearance to that seen after incubation with DL-alpha-aminoadipate and other reported gliotoxins. No evidence of a similar glial-specific action was seen after administration of kainic acid, although extensive neuronal degeneration did result. Incubation of retinas with tritiated glutamate (3H-glu) revealed a selective uptake of the label by Müller cells. Autoradiographic grains were localized over Müller foot processes at the inner limiting membrane, and by 30 minutes labeled the entire glial system. Prior treatment with neurotoxic levels of glutamate did not alter the autoradiographic localization to glial cells. Possible glial-neuronal interactions and their effect on cytotoxic patterns are discussed.

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Glial Cells and Amino Acid Transmitters

Cited by 5 publications

References 24 publications

gamma-Aminobutyric acid directly depolarizes cultured oligodendrocytes

gamma-Aminobutyric acid directly depolarizes cultured oligodendrocytes

Astrocytes support incomplete differentiation of an oligodendrocyte precursor cell.

Glutamate‐induced cellular injury in isolated chick embryo retina: Müller cell localization of initial effects

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