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Статті в журналах з теми "Retinal excitotoxicity"

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Автор: Grafiati

Опубліковано: 10 грудня 2022

Оновлено: 29 січня 2023

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1

Alfarhan, Moaddey, Fang Liu, Shengshuai Shan, Prahalathan Pichavaram, Payaningal R. Somanath, and S. Priya Narayanan. "Pharmacological Inhibition of Spermine Oxidase Suppresses Excitotoxicity Induced Neuroinflammation in Mouse Retina." International Journal of Molecular Sciences 23, no. 4 (February 15, 2022): 2133. http://dx.doi.org/10.3390/ijms23042133.

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Анотація:

Polyamine oxidation plays a major role in neurodegenerative diseases. Previous studies from our laboratory demonstrated that spermine oxidase (SMOX, a member of the polyamine oxidase family) inhibition using MDL 72527 reduced neurodegeneration in models of retinal excitotoxicity and diabetic retinopathy. However, the mechanisms behind the neuroprotection offered by SMOX inhibition are not completely studied. Utilizing the experimental model of retinal excitotoxicity, the present study determined the impact of SMOX blockade in retinal neuroinflammation. Our results demonstrated upregulation in the number of cells positive for Iba-1 (ionized calcium-binding adaptor molecule 1), CD (Cluster Differentiation) 68, and CD16/32 in excitotoxicity-induced retinas, while MDL 72527 treatment reduced these changes, along with increases in the number of cells positive for Arginase1 and CD206. When retinal excitotoxicity upregulated several pro-inflammatory genes, MDL 72527 treatment reduced many of them and increased anti-inflammatory genes. Furthermore, SMOX inhibition upregulated antioxidant signaling (indicated by elevated Nrf2 and HO-1 levels) and reduced protein-conjugated acrolein in excitotoxic retinas. In vitro studies using C8-B4 cells showed changes in cellular morphology and increased reactive oxygen species formation in response to acrolein (a product of SMOX activity) treatment. Overall, our findings indicate that the inhibition SMOX pathway reduced neuroinflammation and upregulated antioxidant signaling in the retina.

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2

Chao, Hsiao-Ming, Ing-Ling Chen, and Jorn-Hon Liu. "S-Allyl L-Cysteine Protects the Retina Against Kainate Excitotoxicity in the Rat." American Journal of Chinese Medicine 42, no. 03 (January 2014): 693–708. http://dx.doi.org/10.1142/s0192415x14500451.

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Анотація:

Excitotoxicity has been proposed to play a pivotal role in retinal ischemia. Retinal ischemia-associated ocular disorders are vision threatening. The aim was to also examine whether and how S-allyl L-cysteine (SAC) can protect the retina against kainate excitotoxicity. In vivo retinal excitotoxicity was induced by an intravitreous injection of 100 μM kainate into a Wistar rat eye for 1 day. The management and mechanisms involved in the processes were evaluated by electrophysiology, immunohistochemistry, histopathology, and various biochemical approaches. In the present study, the cultured retinal cells were shown to possess kainate receptors. The defined retinal excitotoxic changes were characterized by a decrease in electroretinogram (ERG) b-wave amplitudes, a loss of the fluorogold retrograde labeled retinal ganglion cells (RGCs), an increase in the apoptotic cells in the RGC layer, and an increase in vimentin or glial fibrillary acidic protein (GFAP) immunoreactivity, a marker for Müller cells. An up-regulation in the mRNA levels of inducible nitric oxide synthase (iNOS) and matrix metalloproteinases-9 (MMPs-9) was also detected in the retina subjected to kainate excitoxicity. Importantly, the excitotoxicity-induced alterations were significantly blunted when 100 μM SAC and/or the kainate receptor antagonist CNQX was applied. Conclusively, SAC would seem to protect the retina against kainate excitotoxicity via an inhibition of the up-regulation of iNOS and MMP-9 as well as a modulation of glial activation and apoptosis.

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3

Mitori, Hikaru, Takeshi Izawa, Mitsuru Kuwamura, Masahiro Matsumoto, and Jyoji Yamate. "Developing Stage-dependent Retinal Toxicity Induced by l-glutamate in Neonatal Rats." Toxicologic Pathology 44, no. 8 (November 15, 2016): 1137–45. http://dx.doi.org/10.1177/0192623316676424.

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Анотація:

The neurotransmitter glutamate causes excitotoxicity in the human retina. In neonatal rats, the degree of glutamate-induced retinal damage depends on age at administration. To elucidate the sensitivity to glutamate on various developing stage of retina, we investigated glutamate-induced retinal damage and glutamate target cells on each postnatal day (PND). Newborn rats received a single subcutaneous administration of l-glutamate on PNDs 1 to 14. Retinal cell apoptosis characterized as pyknotic and terminal deoxynucleotidyl transferase–mediated dUTP digoxigenin nick end labeling–positive nuclei was analyzed at 6 hr after treatment, and sequential morphological features of retina were evaluated on PND 21. The inner retina on PND 21 exhibited thinning in rats treated after PND 2. The thinning was most severe in rats treated on PND 8 and the number of apoptotic cells also peaked. No thinning was observed in rats treated on PND 14. In the inner nuclear layer, glutamate target cells were mainly amacrine cells; additionally, bipolar cells and horizontal cells were damaged on PND 8. These retinal changes were more severe in central retina than those in peripheral retina on PND 8. Our findings indicate the morphological consequences of glutamate-induced retinal excitotoxicity and glutamate target cells on each PND and reveal that glutamate-induced retinal damage depends on developing stage.

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4

Boccuni, Isabella, and Richard Fairless. "Retinal Glutamate Neurotransmission: From Physiology to Pathophysiological Mechanisms of Retinal Ganglion Cell Degeneration." Life 12, no. 5 (April 25, 2022): 638. http://dx.doi.org/10.3390/life12050638.

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Анотація:

Glutamate neurotransmission and metabolism are finely modulated by the retinal network, where the efficient processing of visual information is shaped by the differential distribution and composition of glutamate receptors and transporters. However, disturbances in glutamate homeostasis can result in glutamate excitotoxicity, a major initiating factor of common neurodegenerative diseases. Within the retina, glutamate excitotoxicity can impair visual transmission by initiating degeneration of neuronal populations, including retinal ganglion cells (RGCs). The vulnerability of RGCs is observed not just as a result of retinal diseases but has also been ascribed to other common neurodegenerative and peripheral diseases. In this review, we describe the vulnerability of RGCs to glutamate excitotoxicity and the contribution of different glutamate receptors and transporters to this. In particular, we focus on the N-methyl-d-aspartate (NMDA) receptor as the major effector of glutamate-induced mechanisms of neurodegeneration, including impairment of calcium homeostasis, changes in gene expression and signalling, and mitochondrial dysfunction, as well as the role of endoplasmic reticular stress. Due to recent developments in the search for modulators of NMDA receptor signalling, novel neuroprotective strategies may be on the horizon.

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5

Boccuni, Isabella, and Richard Fairless. "Retinal Glutamate Neurotransmission: From Physiology to Pathophysiological Mechanisms of Retinal Ganglion Cell Degeneration." Life 12, no. 5 (April 25, 2022): 638. http://dx.doi.org/10.3390/life12050638.

Повний текст джерела

Анотація:

Glutamate neurotransmission and metabolism are finely modulated by the retinal network, where the efficient processing of visual information is shaped by the differential distribution and composition of glutamate receptors and transporters. However, disturbances in glutamate homeostasis can result in glutamate excitotoxicity, a major initiating factor of common neurodegenerative diseases. Within the retina, glutamate excitotoxicity can impair visual transmission by initiating degeneration of neuronal populations, including retinal ganglion cells (RGCs). The vulnerability of RGCs is observed not just as a result of retinal diseases but has also been ascribed to other common neurodegenerative and peripheral diseases. In this review, we describe the vulnerability of RGCs to glutamate excitotoxicity and the contribution of different glutamate receptors and transporters to this. In particular, we focus on the N-methyl-d-aspartate (NMDA) receptor as the major effector of glutamate-induced mechanisms of neurodegeneration, including impairment of calcium homeostasis, changes in gene expression and signalling, and mitochondrial dysfunction, as well as the role of endoplasmic reticular stress. Due to recent developments in the search for modulators of NMDA receptor signalling, novel neuroprotective strategies may be on the horizon.

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6

Vidal-Villegas, Beatriz, Johnny Di Pierdomenico, Juan A. Miralles de Imperial-Ollero, Arturo Ortín-Martínez, Francisco M. Nadal-Nicolás, Jose M. Bernal-Garro, Nicolás Cuenca Navarro, María P. Villegas-Pérez, and Manuel Vidal-Sanz. "Melanopsin+RGCs Are fully Resistant to NMDA-Induced Excitotoxicity." International Journal of Molecular Sciences 20, no. 12 (June 20, 2019): 3012. http://dx.doi.org/10.3390/ijms20123012.

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Анотація:

We studied short- and long-term effects of intravitreal injection of N-methyl-d-aspartate (NMDA) on melanopsin-containing (m+) and non-melanopsin-containing (Brn3a+) retinal ganglion cells (RGCs). In adult SD-rats, the left eye received a single intravitreal injection of 5µL of 100nM NMDA. At 3 and 15 months, retinal thickness was measured in vivo using Spectral Domain-Optical Coherence Tomography (SD-OCT). Ex vivo analyses were done at 3, 7, or 14 days or 15 months after damage. Whole-mounted retinas were immunolabelled for brain-specific homeobox/POU domain protein 3A (Brn3a) and melanopsin (m), the total number of Brn3a+RGCs and m+RGCs were quantified, and their topography represented. In control retinas, the mean total numbers of Brn3a+RGCs and m+RGCs were 78,903 ± 3572 and 2358 ± 144 (mean ± SD; n = 10), respectively. In the NMDA injected retinas, Brn3a+RGCs numbers diminished to 49%, 28%, 24%, and 19%, at 3, 7, 14 days, and 15 months, respectively. There was no further loss between 7 days and 15 months. The number of immunoidentified m+RGCs decreased significantly at 3 days, recovered between 3 and 7 days, and were back to normal thereafter. OCT measurements revealed a significant thinning of the left retinas at 3 and 15 months. Intravitreal injections of NMDA induced within a week a rapid loss of 72% of Brn3a+RGCs, a transient downregulation of melanopsin expression (but not m+RGC death), and a thinning of the inner retinal layers.

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7

Izumi, Yukitoshi, Keiko Shimamoto, Ann M. Benz, Seth B. Hammerman, John W. Olney, and Charles F. Zorumski. "Glutamate transporters and retinal excitotoxicity." Glia 39, no. 1 (May 23, 2002): 58–68. http://dx.doi.org/10.1002/glia.10082.

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8

Milla-Navarro, Santiago, Ariadna Diaz-Tahoces, Isabel Ortuño-Lizarán, Eduardo Fernández, Nicolás Cuenca, Francisco Germain, and Pedro de la Villa. "Visual Disfunction due to the Selective Effect of Glutamate Agonists on Retinal Cells." International Journal of Molecular Sciences 22, no. 12 (June 10, 2021): 6245. http://dx.doi.org/10.3390/ijms22126245.

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Анотація:

One of the causes of nervous system degeneration is an excess of glutamate released upon several diseases. Glutamate analogs, like N-methyl-DL-aspartate (NMDA) and kainic acid (KA), have been shown to induce experimental retinal neurotoxicity. Previous results have shown that NMDA/KA neurotoxicity induces significant changes in the full field electroretinogram response, a thinning on the inner retinal layers, and retinal ganglion cell death. However, not all types of retinal neurons experience the same degree of injury in response to the excitotoxic stimulus. The goal of the present work is to address the effect of intraocular injection of different doses of NMDA/KA on the structure and function of several types of retinal cells and their functionality. To globally analyze the effect of glutamate receptor activation in the retina after the intraocular injection of excitotoxic agents, a combination of histological, electrophysiological, and functional tools has been employed to assess the changes in the retinal structure and function. Retinal excitotoxicity caused by the intraocular injection of a mixture of NMDA/KA causes a harmful effect characterized by a great loss of bipolar, amacrine, and retinal ganglion cells, as well as the degeneration of the inner retina. This process leads to a loss of retinal cell functionality characterized by an impairment of light sensitivity and visual acuity, with a strong effect on the retinal OFF pathway. The structural and functional injury suffered by the retina suggests the importance of the glutamate receptors expressed by different types of retinal cells. The effect of glutamate agonists on the OFF pathway represents one of the main findings of the study, as the evaluation of the retinal lesions caused by excitotoxicity could be specifically explored using tests that evaluate the OFF pathway.

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9

Ishikawa, Makoto. "Abnormalities in Glutamate Metabolism and Excitotoxicity in the Retinal Diseases." Scientifica 2013 (2013): 1–13. http://dx.doi.org/10.1155/2013/528940.

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Анотація:

In the physiological condition, glutamate acts as an excitatory neurotransmitter in the retina. However, excessive glutamate can be toxic to retinal neurons by overstimulation of the glutamate receptors. Glutamate excess is primarily attributed to perturbation in the homeostasis of the glutamate metabolism. Major pathway of glutamate metabolism consists of glutamate uptake by glutamate transporters followed by enzymatic conversion of glutamate to nontoxic glutamine by glutamine synthetase. Glutamate metabolism requires energy supply, and the energy loss inhibits the functions of both glutamate transporters and glutamine synthetase. In this review, we describe the present knowledge concerning the retinal glutamate metabolism under the physiological and pathological conditions.

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10

Youale, Jenny, Karine Bigot, Bindu Kodati, Thara Jaworski, Yan Fan, Nana Yaa Nsiah, Nathaniel Pappenhagen, et al. "Neuroprotective Effects of Transferrin in Experimental Glaucoma Models." International Journal of Molecular Sciences 23, no. 21 (October 22, 2022): 12753. http://dx.doi.org/10.3390/ijms232112753.

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Iron is essential for retinal metabolism, but an excess of ferrous iron causes oxidative stress. In glaucomatous eyes, retinal ganglion cell (RGC) death has been associated with dysregulation of iron homeostasis. Transferrin (TF) is an endogenous iron transporter that controls ocular iron levels. Intraocular administration of TF is neuroprotective in various models of retinal degeneration, preventing iron overload and reducing iron-induced oxidative stress. Herein, we assessed the protective effects of TF on RGC survival, using ex vivo rat retinal explants exposed to iron, NMDA-induced excitotoxicity, or CoCl2-induced hypoxia, and an in vivo rat model of ocular hypertension (OHT). TF significantly preserved RGCs against FeSO4-induced toxicity, NMDA-induced excitotoxicity, and CoCl2-induced hypoxia. TF protected RGCs from apoptosis, ferroptosis, and necrosis. In OHT rats, TF reduced RGC loss by about 70% compared to vehicle-treated animals and preserved about 47% of the axons. Finally, increased iron staining was shown in the retina of a glaucoma patient’s eye as compared to non-glaucomatous eyes. These results indicate that TF can interfere with different cell-death mechanisms involved in glaucoma pathogenesis and demonstrate the ability of TF to protect RGCs exposed to elevated IOP. Altogether, these results suggest that TF is a promising treatment against glaucoma neuropathy.

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11

Tsoka, Pavlina, Paulo R. Barbisan, Keiko Kataoka, Xiaohong Nancy Chen, Bo Tian, Peggy Bouzika, Joan W. Miller, Eleftherios I. Paschalis, and Demetrios G. Vavvas. "NLRP3 inflammasome in NMDA-induced retinal excitotoxicity." Experimental Eye Research 181 (April 2019): 136–44. http://dx.doi.org/10.1016/j.exer.2019.01.018.

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12

Mali, Raghuveer S., Mei Cheng, and Shravan K. Chintala. "Plasminogen activators promote excitotoxicity‐induced retinal damage." FASEB Journal 19, no. 10 (August 2005): 1280–89. http://dx.doi.org/10.1096/fj.04-3403com.

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13

Le, Tam Thi, Tae Kyeom Kang, Ha Thi Do, Trong Duc Nghiem, Wook-Bin Lee, and Sang Hoon Jung. "Protection Against Oxidative Stress-Induced Retinal Cell Death by Compounds Isolated From Ehretia asperula." Natural Product Communications 16, no. 12 (December 2021): 1934578X2110679. http://dx.doi.org/10.1177/1934578x211067986.

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Ehretia asperula ( E asperula) is a well-known traditional medicinal plant in Vietnam with potent activity against a wide range of diseases, including hepatitis B and various cancers. Although E asperula has been used in traditional medicine, the efficacy of E asperula and its bioactive components on retinal degenerative diseases has not been fully evaluated. In present this study, we found that ethanolic extracts of E asperula increased cell viability in retinal precursor cells exposed to glutamate/BSO-induced excitotoxicity/oxidative stress. The major responsible bioactive compounds were rosmarinic acid and methylrosmarinic acid. First, 10 known compounds were isolated from E asperula leaves. Their chemical structures were determined using 1D and 2D nuclear magnetic resonance, and compared with published data. Using high-performance liquid chromatography, we determined the content of 4 compounds in E asperula extract: rosmarinic acid, lithospermic acid B, astragalin, and kaempferol 3-rutinoside. The most abundant of these compounds was lithospermic acid B. The protective effects of the pure compounds and ethanolic extracts against excitotoxicity and oxidative stress-induced retinal cell death were tested in R28 cells. Both 70% and 95% ethanolic extracts of E asperula increased cell viability in these conditions. Rosmarinic acid and methyl rosmarinic acid were more effective at protecting against retinal cell death and elevated reactive oxygen species in cells subjected to glutamate/BSO-induced excitotoxicity/oxidative stress. These findings suggested that E asperula could potentially be used to treat retinal degeneration.

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14

Al-Dbass, Abeer, Musarat Amina, Nawal M. Al Musayeib, Amira A. El-Anssary, Ramesa Shafi Bhat, Rania Fahmy, Majd M. Alhamdan, and Afaf El-Ansary. "Lepidium sativum as candidate against excitotoxicity in retinal ganglion cells." Translational Neuroscience 12, no. 1 (January 1, 2021): 247–59. http://dx.doi.org/10.1515/tnsci-2020-0174.

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Abstract Glutamate excitotoxicity is considered one of the major causes of retinal ganglion cell death in many retinal diseases. Retinal ganglion cell degeneration causes severe blindness since visual signals from the eye to the brain are conducted only through retinal ganglion cells. Objective: We aimed to explore the potential ameliorative effects of L. sativum against glutamate excitotoxicity-induced retinal ganglion cell damage. Methods: Pure retinal ganglion cells were divided into a control group (untreated); L. sativum-treated groups in which retinal ganglion cells were treated with 5, 10, 50, or 100 µg/mL L. sativum seed extract for 2 h; glutamate-treated groups in which cells were treated with 5, 10, 50, or 100 µM glutamate for 48 h; and L. sativum/glutamate groups [pretreatment with L. sativum for 2 h (50 or 100 µg/mL) before glutamate treatment at 100 µM for 48 h]. Cell damage was assessed by comet assay and cell viability was by MTT test. Results: Tailed DNA, tail length, and tail moment of the 50 and 100 mM glutamate-treated groups were significantly greater than those of the blank control group, while the L. sativum-treated groups demonstrated nonsignificantly different tailed DNA, tail length, and tail moment compared with the blank control group, but significantly lower values compared with the glutamate-treated groups. Conclusion: L. sativum ameliorated the cell viability in retinal ganglion cells after high-concentration glutamate exposure. L. sativum seed extracts were efficient anti-excitotoxic and antioxidant agent that might improve the clinical presentation of many neurological disorders.

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15

Zhuang, Dongli, Rong Zhang, Haiyang Liu, and Yi Dai. "A Small Natural Molecule S3 Protects Retinal Ganglion Cells and Promotes Parkin-Mediated Mitophagy against Excitotoxicity." Molecules 27, no. 15 (August 4, 2022): 4957. http://dx.doi.org/10.3390/molecules27154957.

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Анотація:

Glutamate excitotoxicity may contribute to retinal ganglion cell (RGC) degeneration in glaucoma and other optic neuropathies, leading to irreversible blindness. Growing evidence has linked impaired mitochondrial quality control with RGCs degeneration, while parkin, an E3 ubiquitin ligase, has proved to be protective and promotes mitophagy in RGCs against excitotoxicity. The purpose of this study was to explore whether a small molecule S3 could modulate parkin-mediated mitophagy and has therapeutic potential for RGCs. The results showed that as an inhibitor of deubiquitinase USP30, S3 protected cultured RGCs and improved mitochondrial health against NMDA-induced excitotoxicity. Administration of S3 promoted the parkin expression and its downstream mitophagy-related proteins in RGCs. An upregulated ubiquitination level of Mfn2 and protein level of OPA1 were also observed in S3-treated RGCs, while parkin knockdown resulted in a major loss of the protective effect of S3 on RGCs under excitotoxicity. These findings demonstrated that S3 promoted RGC survival mainly through enhancing parkin-mediated mitophagy against excitotoxicity. The neuroprotective value of S3 in glaucoma and other optic neuropathies deserves further investigation.

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16

Ullian, E. M., W. B. Barkis, S. Chen, J. S. Diamond, and B. A. Barres. "Invulnerability of retinal ganglion cells to NMDA excitotoxicity." Molecular and Cellular Neuroscience 26, no. 4 (August 2004): 544–57. http://dx.doi.org/10.1016/j.mcn.2004.05.002.

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17

Liu, Fang, Moaddey Alfarhan, Leanna Baker, Nidhi Shenoy, Yini Liao, Harry O. Henry-Ojo, Payaningal R. Somanath, and S. Priya Narayanan. "Treatment with MDL 72527 Ameliorated Clinical Symptoms, Retinal Ganglion Cell Loss, Optic Nerve Inflammation, and Improved Visual Acuity in an Experimental Model of Multiple Sclerosis." Cells 11, no. 24 (December 16, 2022): 4100. http://dx.doi.org/10.3390/cells11244100.

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Анотація:

Multiple Sclerosis (MS) is a highly disabling neurological disease characterized by inflammation, neuronal damage, and demyelination. Vision impairment is one of the major clinical features of MS. Previous studies from our lab have shown that MDL 72527, a pharmacological inhibitor of spermine oxidase (SMOX), is protective against neurodegeneration and inflammation in the models of diabetic retinopathy and excitotoxicity. In the present study, utilizing the experimental autoimmune encephalomyelitis (EAE) model of MS, we determined the impact of SMOX blockade on retinal neurodegeneration and optic nerve inflammation. The increased expression of SMOX observed in EAE retinas was associated with a significant loss of retinal ganglion cells, degeneration of synaptic contacts, and reduced visual acuity. MDL 72527-treated mice exhibited markedly reduced motor deficits, improved neuronal survival, the preservation of synapses, and improved visual acuity compared to the vehicle-treated group. The EAE-induced increase in macrophage/microglia was markedly reduced by SMOX inhibition. Upregulated acrolein conjugates in the EAE retina were decreased through MDL 72527 treatment. Mechanistically, the EAE-induced ERK-STAT3 signaling was blunted by SMOX inhibition. In conclusion, our studies demonstrate the potential benefits of targeting SMOX to treat MS-mediated neuroinflammation and vision loss.

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18

Izumi, Yukitoshi, Ann M. Benz, Charity O. Kirby, Joann Labruyere, Charles F. Zorumski, Madelon T. Price, and John W. Olney. "An ex vivo rat retinal preparation for excitotoxicity studies." Journal of Neuroscience Methods 60, no. 1-2 (August 1995): 219–25. http://dx.doi.org/10.1016/0165-0270(95)00015-m.

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19

Yang, Ning, Brent K. Young, Ping Wang, and Ning Tian. "The Susceptibility of Retinal Ganglion Cells to Optic Nerve Injury is Type Specific." Cells 9, no. 3 (March 10, 2020): 677. http://dx.doi.org/10.3390/cells9030677.

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Анотація:

Retinal ganglion cell (RGC) death occurs in many eye diseases, such as glaucoma and traumatic optic neuropathy (TON). Increasing evidence suggests that the susceptibility of RGCs varies to different diseases in an RGC type-dependent manner. We previously showed that the susceptibility of several genetically identified RGC types to N-methyl-D-aspartate (NMDA) excitotoxicity differs significantly. In this study, we characterize the susceptibility of the same RGC types to optic nerve crush (ONC). We show that the susceptibility of these RGC types to ONC varies significantly, in which BD-RGCs are the most resistant RGC type while W3-RGCs are the most sensitive cells to ONC. We also show that the survival rates of BD-RGCs and J-RGCs after ONC are significantly higher than their survival rates after NMDA excitotoxicity. These results are consistent with the conclusion that the susceptibility of RGCs to ONC varies in an RGC type-dependent manner. Further, the susceptibilities of the same types of RGCs to ONC and NMDA excitotoxicity are significantly different. These are valuable insights for understanding of the selective susceptibility of RGCs to various pathological insults and the development of a strategy to protect RGCs from death in disease conditions.

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20

Vorwerk, C. K., M. R. Kreutz, T. M. Böckers, M. Brosz, E. B. Dreyer, and B. A. Sabel. "Susceptibility of retinal ganglion cells to excitotoxicity depends on soma size and retinal eccentricity." Current Eye Research 19, no. 1 (January 1999): 59–65. http://dx.doi.org/10.1076/ceyr.19.1.59.5336.

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21

Calvo, Estrella, Santiago Milla-Navarro, Isabel Ortuño-Lizarán, Violeta Gómez-Vicente, Nicolás Cuenca, Pedro De la Villa, and Francisco Germain. "Deleterious Effect of NMDA Plus Kainate on the Inner Retinal Cells and Ganglion Cell Projection of the Mouse." International Journal of Molecular Sciences 21, no. 5 (February 25, 2020): 1570. http://dx.doi.org/10.3390/ijms21051570.

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Анотація:

Combined administration of N-Methyl-D-Aspartate (NMDA) and kainic acid (KA) on the inner retina was studied as a model of excitotoxicity. The right eye of C57BL6J mice was injected with 1 µL of PBS containing NMDA 30 mM and KA 10 mM. Only PBS was injected in the left eye. One week after intraocular injection, electroretinogram recordings and immunohistochemistry were performed on both eyes. Retinal ganglion cell (RGC) projections were studied by fluorescent-cholerotoxin anterograde labeling. A clear decrease of the retinal “b” wave amplitude, both in scotopic and photopic conditions, was observed in the eyes injected with NMDA/KA. No significant effect on the “a” wave amplitude was observed, indicating the preservation of photoreceptors. Immunocytochemical labeling showed no effects on the outer nuclear layer, but a significant thinning on the inner retinal layers, thus indicating that NMDA and KA induce a deleterious effect on bipolar, amacrine and ganglion cells. Anterograde tracing of the visual pathway after NMDA and KA injection showed the absence of RGC projections to the contralateral superior colliculus and lateral geniculate nucleus. We conclude that glutamate receptor agonists, NMDA and KA, induce a deleterious effect of the inner retina when injected together into the vitreous chamber.

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22

Lan, Yu-Wen, Yoko Ishii, Kimberly E. Palmer, Karrah Q. Bristow, Joseph Caprioli, and Jacky M. K. Kwong. "2-Deoxy-D-glucose protects retinal ganglion cells against excitotoxicity." NeuroReport 14, no. 18 (December 2003): 2369–72. http://dx.doi.org/10.1097/00001756-200312190-00016.

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23

Hama, Yasuhiro, Hiroshi Katsuki, Chihiro Suminaka, Toshiaki Kume, and Akinori Akaike. "Chloride-dependent acute excitotoxicity in adult rat retinal ganglion cells." Neuropharmacology 55, no. 5 (October 2008): 677–86. http://dx.doi.org/10.1016/j.neuropharm.2008.06.006.

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24

Hare, William A., and Larry Wheeler. "Experimental Glutamatergic Excitotoxicity in Rabbit Retinal Ganglion Cells: Block by Memantine." Investigative Opthalmology & Visual Science 50, no. 6 (June 1, 2009): 2940. http://dx.doi.org/10.1167/iovs.08-2103.

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25

Lambuk, Lidawani, Igor Iezhitsa, Renu Agarwal, Nor Salmah Bakar, Puneet Agarwal, and Nafeeza Mohd Ismail. "Antiapoptotic effect of taurine against NMDA-induced retinal excitotoxicity in rats." NeuroToxicology 70 (January 2019): 62–71. http://dx.doi.org/10.1016/j.neuro.2018.10.009.

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26

Levytska, H., I. Levytskyi, I. Savytskyi, L. Zaiats, and L. Sarakhan. "Investigation of amino acids’ levels in the vitreous body of experimental animals in regmatogenic retinal detachment." Journal of Education, Health and Sport 11, no. 11 (November 30, 2021): 414–22. http://dx.doi.org/10.12775/jehs.2021.11.11.039.

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Анотація:

The article presents the results of studying the levels of amino acids in the vitreous body of rats with rhegmatogenous retinal detachment at different stages of modeling the pathology (on the 3rd, 5th and 7th day). In animals with modeling RRD, was observed a significant increase in the level of alanine, aspartate, glycine, glutamic acid compared with rats of conditionally intact group; maximum changes in indicators were observed on the 7th day of the study. The obtained data are explained by significant neurochemical changes of the glutamatergic system of the neural retina, which cause excitotoxicity (as a result of massive release of neuronal glutamate) and structural changes. In the study of the level of valine, histidine, tyrosine, phenylalanine and methionine, it was found that these amino acids are not involved in the pathogenesis of RRD, so their level does not change. The obtained experimental data deepen the existing pathophysiological data on the pathogenetic links of rhegmatogenous retinal detachment in the early stages of its progression, which is important for practical ophthalmology to develop effective pharmacotherapy of this disease.

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27

An, Yaqiong, Haibo Li, Mengxiao Wang, Zhaohua Xia, Lexi Ding, and Xiaobo Xia. "Nuclear factor erythroid 2-related factor 2 agonist protects retinal ganglion cells in glutamate excitotoxicity retinas." Biomedicine & Pharmacotherapy 153 (September 2022): 113378. http://dx.doi.org/10.1016/j.biopha.2022.113378.

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28

Vernazza, Stefania, Francesco Oddone, Sara Tirendi, and Anna Maria Bassi. "Risk Factors for Retinal Ganglion Cell Distress in Glaucoma and Neuroprotective Potential Intervention." International Journal of Molecular Sciences 22, no. 15 (July 27, 2021): 7994. http://dx.doi.org/10.3390/ijms22157994.

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Retinal ganglion cells (RGCs) are a population of neurons of the central nervous system (CNS) extending with their soma to the inner retina and with their axons to the optic nerve. Glaucoma represents a group of neurodegenerative diseases where the slow progressive death of RGCs results in a permanent loss of vision. To date, although Intra Ocular Pressure (IOP) is considered the main therapeutic target, the precise mechanisms by which RGCs die in glaucoma have not yet been clarified. In fact, Primary Open Angle Glaucoma (POAG), which is the most common glaucoma form, also occurs without elevated IOP. This present review provides a summary of some pathological conditions, i.e., axonal transport blockade, glutamate excitotoxicity and changes in pro-inflammatory cytokines along the RGC projection, all involved in the glaucoma cascade. Moreover, neuro-protective therapeutic approaches, which aim to improve RGC degeneration, have also been taken into consideration.

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29

Yan, Jing, C. Peter Bengtson, Bettina Buchthal, Anna M. Hagenston, and Hilmar Bading. "Coupling of NMDA receptors and TRPM4 guides discovery of unconventional neuroprotectants." Science 370, no. 6513 (October 8, 2020): eaay3302. http://dx.doi.org/10.1126/science.aay3302.

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Excitotoxicity induced by NMDA receptors (NMDARs) is thought to be intimately linked to high intracellular calcium load. Unexpectedly, NMDAR-mediated toxicity can be eliminated without affecting NMDAR-induced calcium signals. Instead, excitotoxicity requires physical coupling of NMDARs to TRPM4. This interaction is mediated by intracellular domains located in the near-membrane portions of the receptors. Structure-based computational drug screening using the interaction interface of TRPM4 in complex with NMDARs identified small molecules that spare NMDAR-induced calcium signaling but disrupt the NMDAR/TRPM4 complex. These interaction interface inhibitors strongly reduce NMDA-triggered toxicity and mitochondrial dysfunction, abolish cyclic adenosine monophosphate–responsive element–binding protein (CREB) shutoff, boost gene induction, and reduce neuronal loss in mouse models of stroke and retinal degeneration. Recombinant or small-molecule NMDAR/TRPM4 interface inhibitors may mitigate currently untreatable human neurodegenerative diseases.

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30

Kokona, Despina, Panagiota-Christina Georgiou, Mihalis Kounenidakis, Foteini Kiagiadaki, and Kyriaki Thermos. "Endogenous and Synthetic Cannabinoids as Therapeutics in Retinal Disease." Neural Plasticity 2016 (2016): 1–12. http://dx.doi.org/10.1155/2016/8373020.

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The functional significance of cannabinoids in ocular physiology and disease has been reported some decades ago. In the early 1970s, subjects who smokedCannabis sativadeveloped lower intraocular pressure (IOP). This led to the isolation of phytocannabinoids from this plant and the study of their therapeutic effects in glaucoma. The main treatment of this disease to date involves the administration of drugs mediating either the decrease of aqueous humour synthesis or the increase of its outflow and thus reduces IOP. However, the reduction of IOP is not sufficient to prevent visual field loss. Retinal diseases, such as glaucoma and diabetic retinopathy, have been defined as neurodegenerative diseases and characterized by ischemia-induced excitotoxicity and loss of retinal neurons. Therefore, new therapeutic strategies must be applied in order to target retinal cell death, reduction of visual acuity, and blindness. The aim of the present review is to address the neuroprotective and therapeutic potential of cannabinoids in retinal disease.

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31

Wu, Xiuquan, Ya-nan Dou, Zhou Fei, and Fei Fei. "Parkin Prevents Glutamate Excitotoxicity Through Inhibiting NLRP3 Inflammasome in Retinal Ganglion Cells." Neuroscience 478 (December 2021): 1–10. http://dx.doi.org/10.1016/j.neuroscience.2021.09.018.

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32

Kolesnikov, A. V., A. V. Shchul’kin, E. N. Yakusheva, O. I. Barenina, M. G. Uzbekov, V. S. Kudrin, P. M. Klodt, and R. U. Ostrovskaya. "Glutamate excitotoxicity and oxidative stress induced by experimental thrombosis of retinal vessels." Neurochemical Journal 10, no. 2 (April 2016): 151–55. http://dx.doi.org/10.1134/s1819712416020057.

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33

Wehrwein, E. "Acetylcholine Protection of Adult Pig Retinal Ganglion Cells from Glutamate-Induced Excitotoxicity." Investigative Ophthalmology & Visual Science 45, no. 5 (May 1, 2004): 1531–43. http://dx.doi.org/10.1167/iovs.03-0406.

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34

Rego, Ana Cristina, та Catarina R. Oliveira. "Influence of γ-aminobutyric acid on retinal cells excitotoxicity upon glucose deprivation". Neuroscience Research 34, № 1 (травень 1999): 31–36. http://dx.doi.org/10.1016/s0168-0102(99)00030-9.

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35

Dionysopoulou, Stavroula, Per Wikström, Erik Walum, and Kyriaki Thermos. "Effect of NADPH oxidase inhibitors in an experimental retinal model of excitotoxicity." Experimental Eye Research 200 (November 2020): 108232. http://dx.doi.org/10.1016/j.exer.2020.108232.

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36

Vallazza-Deschamps, Géraldine, Céline Fuchs, David Cia, Luc-Henri Tessier, José A. A. Sahel, Henri Dreyfus, and Serge Picaud. "Diltiazem-induced Neuroprotection in Glutamate Excitotoxicity and Ischemic Insult of Retinal Neurons." Documenta Ophthalmologica 110, no. 1 (January 2005): 25–35. http://dx.doi.org/10.1007/s10633-005-7341-1.

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37

Ganesh, Bhagyalaxmi S., and Shravan K. Chintala. "Inhibition of Reactive Gliosis Attenuates Excitotoxicity-Mediated Death of Retinal Ganglion Cells." PLoS ONE 6, no. 3 (March 31, 2011): e18305. http://dx.doi.org/10.1371/journal.pone.0018305.

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38

McMahon, D. G., and L. V. Ponomareva. "Nitric oxide and cGMP modulate retinal glutamate receptors." Journal of Neurophysiology 76, no. 4 (October 1, 1996): 2307–15. http://dx.doi.org/10.1152/jn.1996.76.4.2307.

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1. In the retina, as in other regions of the vertebrate central nervous system, glutamate receptors mediate excitatory chemical synaptic transmission and are a critical site for the regulation of cellular communication. In this study, retinal horizontal cells from the hybrid less were dissociated in cell culture, voltage clamped by the whole cell recording technique, and the currents evoked by application of excitatory amino acids recorded. 2. Responses to glutamate and its agonist kainate were reduced by approximately 50% in the presence of the nitric oxide (NO) donors sodium nitroprusside and S-nitroso-N-acetylpenicillamine. The effect of these compounds was blocked by the NO scavenger hemoglobin. 3. This effect of NO donors on kainate currents could be mimicked by the application of a membrane permeable guanosine 3',5'-cyclic monophosphate (cGMP) analogue, 8-Br-cGMP. The NO effect was also blocked by application of the guanylate cyclase inhibitor LY-83583, and by a protein kinase G inhibitor peptide. 4. In H1-type horizontal cells, stimulation of endogenous nitric oxide synthase with L-arginine reduced kainate responses, whereas application of D-arginine had no effect. 5. This receptor modulation mechanism may act in concert with other pre- and postsynaptic mechanisms to modify horizontal cell synaptic function according to the adaptational state of the retina and also may protect horizontal cells from glutamate excitotoxicity.

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39

Luo, Xiaopeng, Yankun Yu, Zongqin Xiang, Huisu Wu, Seeram Ramakrishna, Yuqiang Wang, Kwok-Fai So, Zaijun Zhang, and Ying Xu. "Tetramethylpyrazine nitrone protects retinal ganglion cells against N -methyl-d -aspartate-induced excitotoxicity." Journal of Neurochemistry 141, no. 3 (March 3, 2017): 373–86. http://dx.doi.org/10.1111/jnc.13970.

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40

Tawarayama, Hiroshi, Qiwei Feng, Namie Murayama, Noriyuki Suzuki, and Toru Nakazawa. "Cyclin-Dependent Kinase Inhibitor 2b Mediates Excitotoxicity-Induced Death of Retinal Ganglion Cells." Investigative Opthalmology & Visual Science 60, no. 13 (October 1, 2019): 4479. http://dx.doi.org/10.1167/iovs.19-27396.

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41

Mitori, Hikaru, Takeshi Izawa, Mitsuru Kuwamura, Masahiro Matsumoto, and Jyoji Yamate. "Gene expression profile in retinal excitotoxicity induced by L-glutamate in neonatal rats." Journal of Toxicologic Pathology 31, no. 4 (2018): 301–6. http://dx.doi.org/10.1293/tox.2018-0026.

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42

Hu, Xinxin, Dongli Zhuang, Rong Zhang, Xinghuai Sun, Qinkang Lu, and Yi Dai. "The small molecule inhibitor PR-619 protects retinal ganglion cells against glutamate excitotoxicity." NeuroReport 31, no. 16 (November 4, 2020): 1134–41. http://dx.doi.org/10.1097/wnr.0000000000001522.

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43

Schlüter, Annabelle, Bahar Aksan, Rossella Fioravanti, Sergio Valente, Antonello Mai, and Daniela Mauceri. "Histone Deacetylases Contribute to Excitotoxicity-Triggered Degeneration of Retinal Ganglion Cells In Vivo." Molecular Neurobiology 56, no. 12 (June 3, 2019): 8018–34. http://dx.doi.org/10.1007/s12035-019-01658-x.

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44

Liu, Hong-li, Fang-Yuan Hu, Ping Xu, and Ji-Hong Wu. "Regulation of mitophagy by metformin improves the structure and function of retinal ganglion cells following excitotoxicity-induced retinal injury." Experimental Eye Research 217 (April 2022): 108979. http://dx.doi.org/10.1016/j.exer.2022.108979.

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45

Mizuno, Fengxia, Peter Barabas, David Krizaj, and Abram Akopian. "Glutamate-induced internalization of Cav1.3 L-type Ca2+channels protects retinal neurons against excitotoxicity." Journal of Physiology 588, no. 6 (March 12, 2010): 953–66. http://dx.doi.org/10.1113/jphysiol.2009.181305.

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46

Rodríguez Villanueva, Javier, Jorge Martín Esteban, and Laura J. Rodríguez Villanueva. "Retinal Cell Protection in Ocular Excitotoxicity Diseases. Possible Alternatives Offered by Microparticulate Drug Delivery Systems and Future Prospects." Pharmaceutics 12, no. 2 (January 24, 2020): 94. http://dx.doi.org/10.3390/pharmaceutics12020094.

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Анотація:

Excitotoxicity seems to play a critical role in ocular neurodegeneration. Excess-glutamate-mediated retinal ganglion cells death is the principal cause of cell loss. Uncontrolled glutamate in the synapsis has significant implications in the pathogenesis of neurodegenerative disorders. The exploitation of various approaches of controlled release systems enhances the pharmacokinetic and pharmacodynamic activity of drugs. In particular, microparticles are secure, can maintain therapeutic drug concentrations in the eye for prolonged periods, and make intimate contact by improving drug bioavailability. According to the promising results reported, possible new investigations will focus intense attention on microparticulate formulations and can be expected to open the field to new alternatives for doctors, as currently required by patients.

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47

Reis, RicardoA M., ClarissaS Schitine, and FernandoG de Mello. "Neurochemical plasticity of Müller cells after retinal injury: overexpression of GAT-3 may potentiate excitotoxicity." Neural Regeneration Research 10, no. 9 (2015): 1376. http://dx.doi.org/10.4103/1673-5374.165224.

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48

Heidinger, Valérie, David Hicks, José Sahel, and Henri Dreyfus. "Peptide growth factors but not ganglioside protect against excitotoxicity in rat retinal neurons in vitro." Brain Research 767, no. 2 (September 1997): 279–88. http://dx.doi.org/10.1016/s0006-8993(97)00605-7.

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49

Sim, Ru Hui, Srinivasa Rao Sirasanagandla, Srijit Das, and Seong Lin Teoh. "Treatment of Glaucoma with Natural Products and Their Mechanism of Action: An Update." Nutrients 14, no. 3 (January 26, 2022): 534. http://dx.doi.org/10.3390/nu14030534.

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Glaucoma is one of the leading causes of irreversible blindness. It is generally caused by increased intraocular pressure, which results in damage of the optic nerve and retinal ganglion cells, ultimately leading to visual field dysfunction. However, even with the use of intraocular pressure-lowering eye drops, the disease still progresses in some patients. In addition to mechanical and vascular dysfunctions of the eye, oxidative stress, neuroinflammation and excitotoxicity have also been implicated in the pathogenesis of glaucoma. Hence, the use of natural products with antioxidant and anti-inflammatory properties may represent an alternative approach for glaucoma treatment. The present review highlights recent preclinical and clinical studies on various natural products shown to possess neuroprotective properties for retinal ganglion cells, which thereby may be effective in the treatment of glaucoma. Intraocular pressure can be reduced by baicalein, forskolin, marijuana, ginsenoside, resveratrol and hesperidin. Alternatively, Ginkgo biloba, Lycium barbarum, Diospyros kaki, Tripterygium wilfordii, saffron, curcumin, caffeine, anthocyanin, coenzyme Q10 and vitamins B3 and D have shown neuroprotective effects on retinal ganglion cells via various mechanisms, especially antioxidant, anti-inflammatory and anti-apoptosis mechanisms. Extensive studies are still required in the future to ensure natural products’ efficacy and safety to serve as an alternative therapy for glaucoma.

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50

Egorov, E. A., V. E. Korelina, D. V. Cherednichenko, and I. R. Gazizova. "Role of neuroinflammation in the pathogenesis of glaucomatous optic neuropathy." Russian Journal of Clinical Ophthalmology 22, no. 2 (2022): 116–21. http://dx.doi.org/10.32364/2311-7729-2022-22-2-116-121.

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This article reviews recent studies on the etiology and pathogenesis of primary open-angle glaucoma (POAG). POAG is now considered a neurodegenerative disease associated with neuroinflammation. Neuroglia plays a key role in the development of neuroinflammation. In impaired homeostasis, microglia is activated to prevent retinal alterations triggered by glutamate excitotoxicity. Macrophages, being still active, release cytokines in the extracellular space and produce matrix metalloproteinases. The result is an increased degradation of collagen fibers of the lamina cribrosa and development of glaucomatous optic neuropathy. Macroglia (astrocytes and Muller cells) are also involved in retinal immunoregulation. Astrocytes produce neurotrophic brain factor which promote the survival of damaged neurons. Additionally, these cells secrete fibrillar proteins that regenerate the extracellular matrix but form a glial scar, thereby inhibiting axonal transport and limiting the regeneration of damaged axons. The activation of microglia and macroglia in glaucoma precedes the loss of retinal ganglion cells. Determining the activity of retinal ganglion cells helps identify specific biomarkers of early glaucoma. Early diagnosis of POAG prevents irreversible damage. The authors discuss potential ways to regulate the activity of glia by stimulating the release of neurotrophic factors and suppressing glia hyperactivity. Keywords: primary open-angle glaucoma, neurodegenerative disease, neuroinflammation, macroglia, microglia, neurotrophic factors. For citation: Egorov E.A., Korelina V.E., Cherednichenko D.V., Gazizova I.R. Role of neuroinflammation in the pathogenesis of glaucomatous optic neuropathy. Russian Journal of Clinical Ophthalmology. 2022;22(2):116–121 (in Russ.). DOI: 10.32364/2311-7729-2022-22-2-116-121

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