Expression of Glutamate and GABA during the Process of Rat Retinal Synaptic Plasticity Induced by Acute High Intraocular Pressure

Zhou, Lihong; Huang, Jufang; Wang, Hui; Luo, Jiayou; Zeng, Leping; Xiong, Kun; Chen, Dan

doi:10.1267/ahc.12029

Cited by 6 publications

(5 citation statements)

References 35 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This indicates that there is a functional reduction of retinal neurons upon I/R injury. Two recent studies, also using the HIOP model in rats, reported the expression and distribution of SYPH after injury [5] , [38] and are consist with our findings of SYPH expression in the INL and OPL ( Fig. 3C ).…”

Section: Discussionsupporting

confidence: 92%

“…3C ). Another study showed that synaptic plasticity can be induced by HIOP in retinas [5] . Therefore, the decrease of synapse-related proteins may also be connected to synaptic plasticity.…”

Section: Discussionmentioning

confidence: 99%

“…Several cellular processes have been linked to retinal degeneration after I/R injury, including glutamate excitotoxicity [3] – [5] , oxidative stress [6] – [8] , and inflammation [9] – [12] . Previous studies have primarily focused on specific processes or pathways; however, the pathogenesis of retinal degeneration after I/R injury is likely the result of interactions between several pathways.…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Identification of Protein Network Alterations upon Retinal Ischemia-Reperfusion Injury by Quantitative Proteomics Using a Rattus norvegicus Model

et al. 2014

View full text Add to dashboard Cite

Retinal ischemia is a common feature associated with several ocular diseases, including diabetic retinopathy. In this study, we investigated the effect of a retinal ischemia and reperfusion (I/R) injury on protein levels via a quantitative shotgun strategy using stable isotope dimethyl labeling combined with LC-MS/MS analysis. Based on the relative quantitation data of 1088 proteins, 234 proteins showed a greater than 1.5-fold change following I/R injury, 194 of which were up-regulated and 40 were down-regulated. Gene ontology analysis revealed that after I/R injury, there was an increase in the metabolic-process related proteins but a decline in cell communication, system process and transport-related proteins. A ribosome protein network and a secreted protein network consisting of many protease inhibitors were identified among the up-regulated proteins, despite a suppression of the mammalian target of rapamycin (mTOR) pathway following the I/R injury. A synaptic-related protein network was found to be significantly down-regulated, implicating a functional reduction of neurons following a retinal I/R injury. Our results provide new systems-biology clues for the study of retinal ischemia.

show abstract

Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Identification of Protein Network Alterations upon Retinal Ischemia-Reperfusion Injury by Quantitative Proteomics Using a Rattus norvegicus Model

et al. 2014

View full text Add to dashboard Cite

show abstract

“…Synaptophysin, a marker of presynaptic terminals, is widely used in the study of synaptic plasticity in the central nervous system and synaptophysin immunoreactivity has been considered to correlate well with synaptogenesis in the central nervous system[ 62 ]. Our previous studies demonstrated that high intraocular pressure-induced retinal injury could result in plastic changes of retinal synapses[ 4 11 63 ]: synaptophysin expression had a distinct spatiotemporal pattern from the inner plexiform layer to the outer plexiform layer and ultrastructure assay detected bouton-like vesicle-containing structures in the outer nuclear layer, however, the presynaptic changes were not accompanied by changes in the postsynaptic components. In this present study, the results of synaptophysin expression in the high intraocular pressure group and the sham surgery group were consistent with our previous study that synaptophysin expression in the inner plexiform layer was initially increased after high intraocular pressure injury and then synaptophysin distribution in the outer plexiform layer spread out, reaching as far as the inner outer nuclear layer with a peak at 7 days.…”

Section: Discussionmentioning

confidence: 99%

Regulatory effects of inhibiting the activation of glial cells on retinal synaptic plasticity

et al. 2014

Self Cite

View full text Add to dashboard Cite

Various retinal injuries induced by ocular hypertension have been shown to induce plastic changes in retinal synapses, but the potential regulatory mechanism of synaptic plasticity after retinal injury was still unclear. A rat model of acute ocular hypertension was established by injecting saline intravitreally for an hour, and elevating the intraocular pressure to 14.63 kPa (110 mmHg). Western blot assay and immunofluorescence results showed that synaptophysin expression had a distinct spatiotemporal change that increased in the inner plexiform layer within 1 day and spread across the outer plexiform layer after 3 days. Glial fibrillary acidic protein expression in retinae was greatly increased after 3 days, and reached a peak at 7 days, which was also consistent with the peak time of synaptophysin expression in the outer plexiform layer following the increased intraocular pressure. Fluorocitrate, a glial metabolic inhibitor, was intravitreally injected to inhibit glial cell activation following high intraocular pressure. This significantly inhibited the enhanced glial fibrillary acidic protein expression induced by high intraocular pressure injury. Synaptophysin expression also decreased in the inner plexiform layer within a day and the widened distribution in the outer plexiform layer had disappeared by 3 days. The results suggested that retinal glial cell activation might play an important role in the process of retinal synaptic plasticity induced by acute high intraocular pressure through affecting the expression and distribution of synaptic functional proteins, such as synaptophysin.

show abstract

“…The retinal tissue preparation was performed as previously described [20]. Briefly, the rats were sacrificed with excessive 2% pentobarbital solution intravitreal injection (80 mg/kg).…”

Section: Retinal Tissue Preparationmentioning

confidence: 99%

Role of vascular endothelial growth factor-165b in the breakdown of the blood-retinal barrier after acute high intraocular pressure in rats

Shen

Liu

et al. 2019

Preprint

View full text Add to dashboard Cite

Background: The blood-retinal barrier (BRB) is essential in maintaining the retinal homeostasis of the microenvironment, previous studies have found that BRB breakdown occurs after acute high intraocular pressure (HIOP) in rats, elevated intraocular pressure can induce upregulation of vascular endothelial growth factor-165b (VEGF-165b) protein in the retina, but the role of VEGF-A165b in BRB breakdown after acute HIOP is still undetermined. Methods: In this study, the rat acute HIOP model was established before and after intravitreous injection of anti-VEGF-165b antibody. The expression of VEGF-165b and ZO-1 in rat retina was detected by immunohistochemistry or western blotting, and the breakdown of BRB was detected by Evans blue (EB) dye. Results: The normal retina of rats expressed VEGF-165b protein, which was mainly located in the retinal ganglion cell (RGC) layer and the inner nuclear layer and was coexpressed with tight junction protein ZO-1. After acute HIOP, the expression of VEGF-165b was upregulated (P < 0.01); The expression of ZO-1 was downregulated (P < 0.01) at 12 h and then recovered at 3 d; EB leakage increased, peaking at 12 h (P < 0.01). After intravitreous injection of anti-VEGF-165b antibody, the expression of VEGF-165b protein was significantly downregulated (P < 0.01); and the downregulation of the expression of ZO-1 was more obvious (P < 0.01); EB leakage became more serious, peaking at 3 d (P < 0.01). EB analysis also showed that EB leakage in the peripheral retina was greater than that in the central retina (P < 0.01). Conclusions: The endogenous VEGF-165b protein may protect the BRB from acute HIOP by regulating the expression of ZO-1. The differential destruction of BRB after acute HIOP may be related to the selective loss of RGCs.

show abstract

Expression of Glutamate and GABA during the Process of Rat Retinal Synaptic Plasticity Induced by Acute High Intraocular Pressure

Cited by 6 publications

References 35 publications

Identification of Protein Network Alterations upon Retinal Ischemia-Reperfusion Injury by Quantitative Proteomics Using a Rattus norvegicus Model

Identification of Protein Network Alterations upon Retinal Ischemia-Reperfusion Injury by Quantitative Proteomics Using a Rattus norvegicus Model

Regulatory effects of inhibiting the activation of glial cells on retinal synaptic plasticity

Role of vascular endothelial growth factor-165b in the breakdown of the blood-retinal barrier after acute high intraocular pressure in rats

Contact Info

Product

Resources

About