Swelling of Müller cells induced by AP3 and glutamate transport substrates in rat retina

Izumi, Yukitoshi; Kirby-Sharkey, Charity O.; Benz, Ann; Mennerick, Steven; Labruyere, Joan; Price, Madelon T.; Olney, John W.; Zorumski, Charles F.

doi:10.1002/(sici)1098-1136(199608)17:4<285::aid-glia3>3.0.co;2-z

Cited by 25 publications

(25 citation statements)

References 39 publications

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“…Until now, only a glutamate-evoked swelling of retinal glial cells has been described. It occurred after longer incubation time periods (at least 1 hr) and is thought to be mediated by the Na ϩ transport that drives the uptake of glutamate (Izumi et al, 1996). Likewise, elevated extracellular K ϩ has been shown to cause astrocytic cell swelling (Syková and Orkand, 1980;Walz and Hinks, 1985;Anderova et al, 2001;MacVicar et al, 2002).…”

Section: Mechanism Of Glial Cell Morphological Alterationsmentioning

confidence: 99%

“…Cell volume alterations are important, particularly under pathological conditions such as epilepsy and ischemia in which overexcited neurons release large amounts of glutamate and K ϩ (Adachi et al, 1972;Glass and Dragunow, 1995;Nicholson and Syková, 1998). Increased extracellular glutamate may evoke slow swelling of retinal glial cells resulting from the influx of Na ϩ , which drives the glial glutamate transporters (Izumi et al, 1996), and high K ϩ may cause swelling of astrocytes mediated by the Na-K-2Cl cotransport (Walz and Hinks, 1985;MacVicar et al, 2002). Spreading depression, a profound transient and progressing depolarization of neurons and glia (Somjen, 2001), is accompanied by cell swelling and can be blocked by antagonists of NMDA receptors, whereas blockers of AMPA-kainate receptors are essentially ineffective (Anderson and Andrew, 2002).…”

Section: Introductionmentioning

confidence: 99%

“…With the exceptions of the relatively slow glutamate-evoked swelling of glial cells (Izumi et al, 1996) induced by glutamate-evoked neuronal cell swelling. At least one other neurotransmitter, dopamine, exerts a similar effect on retinal cell morphology.…”

Section: Introductionmentioning

confidence: 99%

“…With the exceptions of the relatively slow glutamate-evoked swelling of glial cells (Izumi et al, 1996) and the cell volume changes during spreading depression, little is known about fast neurotransmitter-induced morphological alterations of glial and neuronal cells in the normal vertebrate retina. Here we show that retinal glial cells quickly and strongly change their shape when glutamate is applied to retinal whole mounts and that this effect is induced by glutamate-evoked neuronal cell swelling.…”

Section: Introductionmentioning

confidence: 99%

“…Increased extracellular glutamate may evoke slow swelling of retinal glial cells resulting from the influx of Na ϩ , which drives the glial glutamate transporters (Izumi et al, 1996), and high K ϩ may cause swelling of astrocytes mediated by the Na-K-2Cl cotransport (Walz and Hinks, 1985;MacVicar et al, 2002). Spreading depression, a profound transient and progressing depolarization of neurons and glia (Somjen, 2001), is accompanied by cell swelling and can be blocked by antagonists of NMDA receptors, whereas blockers of AMPA-kainate receptors are essentially ineffective (Anderson and Andrew, 2002).With the exceptions of the relatively slow glutamate-evoked swelling of glial cells (Izumi et al, 1996) induced by glutamate-evoked neuronal cell swelling. At least one other neurotransmitter, dopamine, exerts a similar effect on retinal cell morphology.…”

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confidence: 99%

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Glutamate-Evoked Alterations of Glial and Neuronal Cell Morphology in the Guinea Pig Retina

Uckermann¹,

Vargová²,

Ulbricht³

et al. 2004

J. Neurosci.

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Neuronal activity is accompanied by transmembranous ion fluxes that cause cell volume changes. In whole mounts of the guinea pig retina, application of glutamate resulted in fast swelling of neuronal cell bodies in the ganglion cell layer (GCL) and the inner nuclear layer (INL) (by ϳ40%) and a concomitant decrease of the thickness of glial cell processes in the inner plexiform layer (IPL) (by ϳ40%) that was accompanied by an elongation of the glial cells, by a thickening of the whole retinal tissue, and by a shrinkage of the extracellular space (by ϳ18%). The half-maximal effect of glutamate was observed at ϳ250 M, after ϳ4 min. The swelling was caused predominantly by AMPAkainate receptor-mediated influx of Na ϩ into retinal neurons. Similar but transient morphological alterations were induced by high K ϩ and dopamine, which caused release of endogenous glutamate and subsequent activation of AMPA-kainate receptors. Apparently, retinal glutamatergic transmission is accompanied by neuronal cell swelling that causes compensatory morphological alterations of glial cells. The effect of dopamine was elicitable only during light adaptation but not in the dark, and glutamate and high K ϩ induced stronger effects in the dark than in the light. This suggests that not only the endogenous release of dopamine but also the responsiveness of glutamatergic neurons to dopamine is regulated by light-dark adaptation. Similar morphological alterations (neuronal swelling and decreased glial process thickness) were observed in whole mounts isolated immediately after experimental retinal ischemia, suggesting an involvement of AMPA-kainate receptor activation in putative neurotoxic cell swelling in the postischemic retina.Key words: glutamate; dopamine; ATP; neuroglia; circadian phase; ischemia; retina IntroductionGlial cells play crucial roles in supporting neuronal survival and information processing (Newman and Reichenbach, 1996): they regulate the extracellular homeostasis of relevant ions including K ϩ , control the water content of the extracellular space, and mediate the rapid termination of neuronal activity by transmitter uptake from the synaptic cleft (Matsui et al., 1999). In the retina, neuronally released K ϩ , water, and glutamate are cleared from the extracellular space mainly by the radial glial (Müller) cells. Retinal glial cells display a complex pattern of K ϩ channel expression in their plasma membranes that directs the flow of neuronally released K ϩ into the glial cell bodies and farther into the vitreous and the blood vessels (Kofuji et al., 2002). Parallel water fluxes were suggested to be coupled to the transglial K ϩ fluxes (Nagelhus et al., 1999). The K ϩ and water fluxes, generated by neuronal activity and mediated by glial cells, are accompanied by swelling of cells and shrinkage of the extracellular space caused by the decreased extracellular osmolality (Dietzel et al., 1980;Jendelová and Syková, 1991;Syková, 1991). Cell volume alterations are important, particularly under pathological conditions such as ...

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Section: Mechanism Of Glial Cell Morphological Alterationsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

mentioning

confidence: 99%

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Glutamate-Evoked Alterations of Glial and Neuronal Cell Morphology in the Guinea Pig Retina

Uckermann¹,

Vargová²,

Ulbricht³

et al. 2004

J. Neurosci.

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Ionic mechanisms in glutamate-induced astrocyte swelling: Role of K+ influx

Bender

Schousboe²,

Reichelt

et al. 1998

J. Neurosci. Res.

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L-Glutamate (L-GLU) induced astrocyte swelling in a time- and concentration-dependent, as well as Na+- and Ca2+-dependent, and Cl(-)-independent manner. Swelling was prevented by MK-801, cystine, and ouabain. Since L-GLU swelling is ionically dependent, we determined the role of various ions in such swelling. Our results indicate that K+ uptake plays a major role in the mechanism of L-GLU-induced astrocyte swelling. Like swelling, K+ uptake is dependent on Ca2+ and Na+, but not on Cl-. Likewise, K+ uptake was inhibited by MK-801, cystine, and ouabain. The K+ channel blockers, Ba2+ and tetraethylammonium, partially prevented L-GLU-induced swelling. In addition to K+ channels, K+ influx may also be mediated through Na+/K+-ATPase, as its activity is increased by L-GLU uptake along with the required Na+. Taken together, the data suggest that K+ influx plays a key role in the mechanism of L-GLU-mediated astrocyte swelling.

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

Heidinger

Dreyfus

Sahel

et al. 1998

Glia

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Swelling of Müller cells induced by AP3 and glutamate transport substrates in rat retina

Cited by 25 publications

References 39 publications

Glutamate-Evoked Alterations of Glial and Neuronal Cell Morphology in the Guinea Pig Retina

Glutamate-Evoked Alterations of Glial and Neuronal Cell Morphology in the Guinea Pig Retina

Ionic mechanisms in glutamate-induced astrocyte swelling: Role of K+ influx

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

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