动物造模,青光眼动物模型 zi-bio 2024-03-04 935

　　Background: The synapses of retinal ganglion cell dendrites (RGCs) at the axonal terminals of bipolar cells in the inner reticulum layer (IPL). The changes in dendrites and synapses of bipolar cells in the inner retina may severely impair the function of retinal ganglion cells in RGC glaucoma. Recently, synaptic plasticity has been observed in the adult central nervous system, including the outer retinal layer. However, little attention has been paid to the synaptic changes between RGCs and bipolar cells in glaucoma. We induced a high intraocular pressure (IOP) model in rats by burning the scleral vein. After the increase of intraocular pressure (IOP), we investigated the changes in synaptic structure and protein expression in the inner layer of the retina at different time points.

　　Result: Synaptin, a synaptic vesicle protein, increases throughout the entire IPL, outer plexiform layer, and outer nuclear layer when intraocular pressure increases. After elevated intraocular pressure, the expression of synapsin in the innermost IPL bipolar cells increases. After 1 and 4 weeks of elevated intraocular pressure, the expression of synapsin in RGC, SMI-32, and RGC dendrites significantly increased. After Western blot analysis, both synapsin and synaptic vesicle protein increased after elevated intraocular pressure. By using a perspective microscope, the IPL ribbon synapses in retinal slices were quantified and structurally evaluated, and the total number of ribbon synapses decreased with increased intraocular pressure. After the increase of intraocular pressure, the diameter and number of synaptic vesicles increase, while the length of the activation zone and the number of vesicles decrease.

　　Conclusion: The total number of synapses decreases with the decrease of dendrites in retinal ganglion cells after elevated intraocular pressure. After inducing glaucoma, synaptic vesicle proteins and immature synapses attempt to increase between bipolar cells and RGCs in the inner layer of the retina.

　　Keywords: retinal ganglion cells, glaucoma synapses

　　Background: Glaucoma is a neurodegenerative disease characterized by the death of retinal ganglion cells (RGCs). In glaucoma patients and experimental models, retinal ganglion cells undergo apoptosis. Many studies have shown that elevated chronic intraocular pressure (IOP) is a clinical characteristic of glaucoma, leading to a decrease in cell size, dendritic contraction, and loss of RGC dendritic branches before cell apoptosis. The dendritic structure of glaucoma determines the function of visual processing of retinal ganglion cells. Changes in dendritic morphology occur before cell death, and studying the changes in dendritic cells is a key focus in understanding the pathophysiology of glaucoma. RGC dendritic synapses are located at the axonal terminals of the inner reticulum layer (IPL) bipolar cells. The early changes in RGC dendritic structure may have a significant impact on synaptic transmission efficiency. Before the loss of RGC function in glaucoma, there may be functional deficiencies. However, there have been few studies on the synaptic changes between RGCs and bipolar cells in glaucoma.

　　Due to the inability of axons in the adult central nervous system to regenerate after injury, the growth of retinal ganglion cell axons will be greatly slowed down after birth. However, unlike axons, RGC dendrites are a reactive element. It has been proven that damaged dendrites can increase their dendritic receptive field and develop new dendritic branches. Recent reports have shown that dendrites and synapses of adult central nervous system neurons have plasticity, including the retina. For example, retinal tissue obtained from age-related macular degeneration patients