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Alterations of the synapse of the inner retinal layers after chronic intraocular pressure elevation in glaucoma animal model

机译：青光眼动物模型中慢性眼内压升高后视网膜内层突触的改变

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Background Dendrites of retinal ganglion cells (RGCs) synapse with axon terminals of bipolar cells in the inner plexiform layer (IPL). Changes in RGC dendrites and synapses between bipolar cells in the inner retinal layer may critically alter the function of RGCs in glaucoma. Recently, synaptic plasticity has been observed in the adult central nervous system, including the outer retinal layers. However, few studies have focused on changes in the synapses between RGCs and bipolar cells in glaucoma. In the present study, we used a rat model of ocular hypertension induced by episcleral vein cauterization to investigate changes in synaptic structure and protein expression in the inner retinal layer at various time points after moderate intraocular pressure (IOP) elevation. Results Synaptophysin, a presynaptic vesicle protein, increased throughout the IPL, outer plexiform layer, and outer nuclear layer after IOP elevation. Increased synaptophysin after IOP elevation was expressed in bipolar cells in the innermost IPL. The RGC marker, SMI-32, co-localized with synaptophysin in RGC dendrites and were significantly increased at 1 week and 4 weeks after IOP elevation. Both synaptophysin and postsynaptic vesicle protein, PSD-95, were increased after IOP elevation by western blot analysis. Ribbon synapses in the IPL were quantified and structurally evaluated in retinal sections by transmission electron microscopy. After IOP elevation the total number of ribbon synapses decreased. There were increases in synapse diameter and synaptic vesicle number and decreases in active zone length and the number of docked vesicles after IOP elevation. Conclusions Although the total number of synapses decreased as RGCs were lost after IOP elevation, there are attempts to increase synaptic vesicle proteins and immature synapse formation between RGCs and bipolar cells in the inner retinal layers after glaucoma induction.
机译：视网膜神经节细胞（RGC）的背景树突与内部丛状层（IPL）中双极细胞的轴突末端突触。视网膜内层中双极细胞之间RGC树突和突触的变化可能会严重改变青光眼中RGC的功能。最近，在成年的中枢神经系统，包括视网膜的外层，已经观察到突触可塑性。然而，很少有研究集中在青光眼的RGC和双极细胞之间的突触变化。在本研究中，我们使用了由巩膜静脉烧灼诱发的高眼压大鼠模型，以研究中度眼内压（IOP）升高后各个时间点内视网膜层突触结构和蛋白质表达的变化。结果突触前素（一种突触前囊泡蛋白）在IOP升高后整个IPL，外丛状层和外核层均增加。在最内层IPL的双极细胞中，眼压升高后突触素增加。 RGC标记SMI-32与突触素共定位于RGC树突中，并在IOP升高后1周和4周显着增加。通过蛋白质印迹分析，眼压升高后，突触素和突触后囊泡蛋白PSD-95均增加。通过透射电子显微镜对IPL中的带状突触进行定量并在视网膜切片中对其结构进行评估。眼压升高后，带状突触的总数减少。眼压升高后，突触直径和突触小泡数目增加，活动区长度和对接小泡数目减少。结论尽管IOP升高后，随着RGC的丢失，突触的总数减少，但仍存在尝试增加青光眼诱导后视网膜内层中RGC与双极细胞之间突触小泡蛋白的增加和突触形成的不成熟的尝试。

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