The dendrites of retinal ganglion cells (RGCs) synapse with the axon terminals of bipolar cells in the inner plexiform layer (IPL). Changes in the RGC dendrites and synapses between the bipolar cells in the inner retinal layer may critically alter the function of RGCs in glaucoma. The present study attempted to discover changes in the synapse using brain-derived neurotrophic factor (BDNF) after glaucoma induction by chronic intraocular pressure elevation in a rat model. Immunohistochemical staining revealed that the BDNF-injected group had a significant increase in the level of synaptophysin, which is a presynaptic vesicle protein, in the innermost IPL compared with the phosphate-buffered saline (PBS)-injected group. SMI-32, which is a marker of RGCs, was colocalized with synaptophysin in RGC dendrites, and this colocalization significantly increased in the BDNF-injected group. After the induction of glaucoma, the BDNF-injected group exhibited increases in the total number of ribbon synapses, as seen using electron microscopy. Expression of calcium/calmodulin-dependent protein kinase II (CaMKII), cAMP-response element binding protein (CREB) and F-actin, which are key molecules involved in synaptic changes were upregulated after BDNF injection. These initial findings show the capability of BDNF to induce beneficial synaptic changes in glaucoma.

中文翻译：

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在青光眼动物模型中，慢性眼内压升高和脑源性神经营养因子调节后，参与突触可塑性的突触蛋白水平增加。

视网膜神经节细胞（RGC）的树突与内部丛状层（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。本研究试图通过慢性眼内压升高在青光眼诱导后使用脑源性神经营养因子（BDNF）发现突触的变化。免疫组织化学染色显示，与磷酸盐缓冲液（PBS）注射组相比，注射BDNF的组在最内侧IPL的突触素水平显着增加，突触前囊泡蛋白是突触前囊泡蛋白。SMI-32是RGC的标志物，在RGC树突中与突触素共定位，在BDNF注射组中这种共定位显着增加。用电子显微镜观察，诱导青光眼后，注射BDNF的组显示带状突触总数增加。BDNF注射后，上调钙/钙调蛋白依赖性蛋白激酶II（CaMKII），cAMP反应元件结合蛋白（CREB）和F-肌动蛋白的表达，这是涉及突触变化的关键分子。这些初步发现表明，BDNF具有诱导青光眼有益的突触变化的能力。BDNF注射后，与突触变化有关的关键分子cAMP-反应元件结合蛋白（CREB）和F-肌动蛋白被上调。这些初步发现表明，BDNF具有诱导青光眼有益的突触变化的能力。BDNF注射后，与突触变化有关的关键分子cAMP反应元件结合蛋白（CREB）和F-肌动蛋白被上调。这些初步发现表明，BDNF具有诱导青光眼有益的突触变化的能力。