α‐Luminol prevents decreases in glutamate, glutathione, and glutamine synthetase in the retinas of glaucomatous DBA/2J mice

Gionfriddo, Juliet R.; Freeman, Kate S.; Groth, A. M.; Scofield, Virginia L.; Alyahya, Khaleel; Madl, James E.

doi:10.1111/j.1463-5224.2009.00722.x

Cited by 22 publications

(26 citation statements)

References 40 publications

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“…A decline in glutamine synthetase expression and activity was also observed under ischemic, inflammatory, and traumatic conditions, and in glaucoma (Nishiyama et al, 2000; Kruchkova et al, 2001; Moreno et al, 2005). Downregulation of the glutamine synthetase results in a depletion of neuronal glutamate (Gionfriddo et al, 2009). No alterations, or even a slight enhancement, in the glutamine synthetase expression in Müller cells was observed in diabetic retinopathy and after optic nerve crush (Mizutani et al, 1998; Lo et al, 2001; Chen and Weber, 2002; Gerhardinger et al, 2005; but, see Yu et al, 2009).…”

Section: Glutamate Uptake and Metabolismmentioning

confidence: 99%

GABA and Glutamate Uptake and Metabolism in Retinal Glial (Müller) Cells

Bringmann¹,

Grosche²,

Pannicke³

et al. 2013

Front. Endocrinol.

133

123

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Müller cells, the principal glial cells of the retina, support the synaptic activity by the uptake and metabolization of extracellular neurotransmitters. Müller cells express uptake and exchange systems for various neurotransmitters including glutamate and γ-aminobutyric acid (GABA). Müller cells remove the bulk of extracellular glutamate in the inner retina and contribute to the glutamate clearance around photoreceptor terminals. By the uptake of glutamate, Müller cells are involved in the shaping and termination of the synaptic activity, particularly in the inner retina. Reactive Müller cells are neuroprotective, e.g., by the clearance of excess extracellular glutamate, but may also contribute to neuronal degeneration by a malfunctioning or even reversal of glial glutamate transporters, or by a downregulation of the key enzyme, glutamine synthetase. This review summarizes the present knowledge about the role of Müller cells in the clearance and metabolization of extracellular glutamate and GABA. Some major pathways of GABA and glutamate metabolism in Müller cells are described; these pathways are involved in the glutamate-glutamine cycle of the retina, in the defense against oxidative stress via the production of glutathione, and in the production of substrates for the neuronal energy metabolism.

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Section: Glutamate Uptake and Metabolismmentioning

confidence: 99%

GABA and Glutamate Uptake and Metabolism in Retinal Glial (Müller) Cells

Bringmann¹,

Grosche²,

Pannicke³

et al. 2013

Front. Endocrinol.

133

123

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“…Reduced glutamate disrupted important anti-oxidant systems, making oxidative stress secondary to glutamate dysregulation a potential mechanism of RGC loss in glaucoma. In support of this concept, anti-oxidant treatment -luminol restored glutamate, glutamine and GS levels and protected RGCs in the DBA/2J mouse model of glaucoma (Gionfriddo et al, 2009). Further detail regarding the role of oxidative stress appears in the Müller glia section below.…”

Section: Astrocytesmentioning

confidence: 92%

Manipulating Glia to Protect Retinal Ganglion Cells in Glaucoma

Inman¹,

Lupien²,

Horner³

2011

Glaucoma - Current Clinical and Research Aspects

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“…98 The immunohistochemical distribution of glutathione, glutamine synthetase, and glutamate was examined in normal C57BL/6 mice (negative control), glaucomatous DBA2J mice ( positive control), and glaucomatous DBA/2J mice treated with Galavit. 99 Serial sections were immunogold stained for glutamate, glutamine synthetase, and total glutathione, followed by image analysis for staining patterns and density. Focal decreases in glutamate immunostaining were common in the inner nuclear layer of glaucomatous DBA/2J retinas, but not in C57BL/6 or Galavit-treated glaucomatous DBA/2J retinas.…”

Section: Potential Applications Of Free Radical Scavengers In Glaucomamentioning

confidence: 99%

Oxidative stress and potential applications of free radical scavengers in glaucoma

2013

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Glaucoma is the leading cause of irreversible blindness in industrialized countries and comprises a group of diseases characterized by progressive optic nerve degeneration. Glaucoma is commonly associated with elevated intraocular pressure due to impaired outflow of aqueous humor resulting from abnormalities within the drainage system of the anterior chamber angle (open-angle glaucoma) or impaired access of aqueous humor to the drainage system (angle-closure glaucoma). Oxidative injury and altered antioxidant defense mechanisms in glaucoma appear to play a role in the pathophysiology of glaucomatous neurodegeneration that is characterized by death of retinal ganglion cells. Oxidative protein modifications occurring in glaucoma serve as immunostimulatory signals and alter neurosupportive and immunoregulatory functions of glial cells. Initiation of the apoptotic cascade observed in glaucomatous retinopathy can involve oxidant mechanisms and different agents have been shown to be neuroprotective. This review focuses on the molecular mechanisms of oxidant injury and summarizes studies that have investigated novel free radical scavengers in the treatment of glaucomatous neurodegeneration.

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α‐Luminol prevents decreases in glutamate, glutathione, and glutamine synthetase in the retinas of glaucomatous DBA/2J mice

Cited by 22 publications

References 40 publications

GABA and Glutamate Uptake and Metabolism in Retinal Glial (Müller) Cells

GABA and Glutamate Uptake and Metabolism in Retinal Glial (Müller) Cells

Manipulating Glia to Protect Retinal Ganglion Cells in Glaucoma

Oxidative stress and potential applications of free radical scavengers in glaucoma

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