Excitotoxic damage of retinal glial cells depends upon normal neuron‐glial interactions

Excitotoxic damage of retinal glial cells depends upon normal neuron‐glial interactions Glutamate, the principal retinal neurotransmitter, can also act as a toxin when present in excessive concentrations as may occur in pathologies such as retinal ischemia or more generally in cerebral neuronal degenerative disease. As glial cells play pivotal roles in transfer of blood‐borne molecules and in glutamate clearance, we investigated the effects of the excitatory amino acids glutamic and kainic acid on different in vitro preparations of retinal Müller glial cells. Glial viability or morphology were not influenced by excitatory amino acid exposure in either pure glial cultures or in monolayer cultures of mixed neonatal neurons and glia, whereas kainic acid specifically lysed amacrine cells in mixed or pure neuronal cultures. When retinal fragments were pre‐incubated in excitatory amino acids prior to dissociation and seeding into culture, under these conditions Müller glial cells exhibited a dramatic loss of their normal epithelioid form to a retracted morphology. However, glial cell viability was not compromised, and rapid restoration of epithelioid in vitro glial morphology could be achieved by addition of exogenous epidermal and basic fibroblast growth factor to the culture medium. This study demonstrates that glial cells are structurally perturbed by excitotoxic conditions and that such effects are dependent on normal glial‐neuronal interactions. GLIA 23:150–159, 1998. © 1998 Wiley‐Liss, Inc. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Glia Wiley

Excitotoxic damage of retinal glial cells depends upon normal neuron‐glial interactions

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Publisher
Wiley
Copyright
Copyright © 1998 Wiley‐Liss, Inc.
ISSN
0894-1491
eISSN
1098-1136
D.O.I.
10.1002/(SICI)1098-1136(199806)23:2<146::AID-GLIA6>3.0.CO;2-4
Publisher site
See Article on Publisher Site

Abstract

Glutamate, the principal retinal neurotransmitter, can also act as a toxin when present in excessive concentrations as may occur in pathologies such as retinal ischemia or more generally in cerebral neuronal degenerative disease. As glial cells play pivotal roles in transfer of blood‐borne molecules and in glutamate clearance, we investigated the effects of the excitatory amino acids glutamic and kainic acid on different in vitro preparations of retinal Müller glial cells. Glial viability or morphology were not influenced by excitatory amino acid exposure in either pure glial cultures or in monolayer cultures of mixed neonatal neurons and glia, whereas kainic acid specifically lysed amacrine cells in mixed or pure neuronal cultures. When retinal fragments were pre‐incubated in excitatory amino acids prior to dissociation and seeding into culture, under these conditions Müller glial cells exhibited a dramatic loss of their normal epithelioid form to a retracted morphology. However, glial cell viability was not compromised, and rapid restoration of epithelioid in vitro glial morphology could be achieved by addition of exogenous epidermal and basic fibroblast growth factor to the culture medium. This study demonstrates that glial cells are structurally perturbed by excitotoxic conditions and that such effects are dependent on normal glial‐neuronal interactions. GLIA 23:150–159, 1998. © 1998 Wiley‐Liss, Inc.

Journal

GliaWiley

Published: Jun 1, 1998

References

  • Expression of NMDA and high‐affinity kainate receptor subunit mRNAs in the adult rat retina
    Brändstatter, Brändstatter; Hartveit, Hartveit; Sassoe‐Pognetto, Sassoe‐Pognetto; Wässle, Wässle
  • The excitatory neurotransmitter glutamate causes filopodia formation in cultured hippocampal astrocytes
    Cornell‐Bell, Cornell‐Bell; Thomas, Thomas; Smith, Smith
  • Glial calcium
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  • Glutamate: a neurotransmitter in mammalian brain
    Fonnum, Fonnum
  • Quisqualate‐induced excitotoxic death of glial cells: Transient vulnerability of cultured astrocytes
    Haas, Haas; Erdö, Erdö
  • Peptide growth factors but not ganglioside protect against excitotoxicity in rat retinal neurons in vitro
    Heidinger, Heidinger; Hicks, Hicks; Sahel, Sahel; Dreyfus, Dreyfus
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    Huxlin, Huxlin; Dreher, Dreher; Schultz, Schultz; Dreher, Dreher
  • The early reactions of non‐neuronal cells to brain injury
    Landis, Landis
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    Pin, Pin; Duvoisin, Duvoisin
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    Rothman, Rothman; Olney, Olney
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    Zeevalk, Zeevalk; Hyndman, Hyndman; Nicklas, Nicklas

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