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.

The aims of this study are to investigate the clinical characteristics of patients with anterior hypertensive uveitis and to compare the characteristics between patients in cytomegalovirus (CMV)-positive and CMV-negative groups in their aqueous humor samples. Immunocompetent patients (n = 42) with a history of chronic and/or recurrent hypertensive anterior uveitis underwent ophthalmic examination and serological tests. Among the 42 patients with hypertensive anterior uveitis, aqueous humor sampling was performed in 21, and they were analyzed for viral deoxyribonucleic acids using the polymerase chain reaction (PCR). The average age of the 42 patients with hypertensive anterior uveitis was 57.6 years, and 29 (69.0 %) of the subjects were males. Of the patients, 22 (52.4 %) underwent glaucoma surgery, and the average corneal endothelial cell counts were 1908 cells/mm2. Among the 21 patients who underwent an aqueous sampling, 6 were positive for CMV-DNA, while 15 were negative. The frequency of glaucoma surgery was similar between groups (CMV positive vs. CMV negative, 66.0 vs. 66.0 %, P = 0.701). However, 66.7 % of the CMV-positive group underwent glaucoma tube shunt surgery, whereas 80 % of the CMV-negative group underwent trabeculectomy or received an ExPRESS glaucoma filtration device (Alcon, Fort Worth, TX) for glaucoma surgery (P = 0.095). The corneal endothelial cell counts were significantly lower in the CMV-positive group (CMV positive vs. CMV negative, 1245 ± 560 vs. 1981 ± 387 cells/mm2; P = 0.009). CMV was found to be an etiological factor in patients with hypertensive anterior uveitis in Korea. Special caution is needed for patients with CMV-induced hypertensive anterior uveitis, considering its adverse effect on the corneal endothelium.

There is increasing evidence that autonomic dysfunction is an important factor in the progression of glaucoma. Mechanism of the association between autonomic dysfunction and progression of glaucoma is poorly understood. Since blood circulation is basically regulated by the autonomic nervous system, autonomic dysfunction may contribute to unstable or fluctuating blood pressure. Therefore, It is hypothesized that autonomic dysfunction may contribute to impaired ocular blood flow and lead to glaucoma progression. However, no clinical study yet has evaluated the relationship between ocular blood flow and autonomic nervous function. We enrolled 152 open angle glaucoma patient. Ocular blood flow was assessed by measuring vessel density (VD) using optical coherence tomography angiography, and autonomic nervous function was evaluated with heart-rate variability (HRV) parameters. The low frequency/high frequency (LF/HF) ratio, which is one of the HRV parameters, quantified the degree of sympathovagal balance. This indicator could represent autonomic dysfunction. Higher LF/HF ratio was associated with reduction of the deep parapapillary VD (R = − 0.243, P = 0.003). Linear regression analysis showed a significant negative association between parapapillary choroidal VD and LF/HF ratio (β = − 0.249; 95% confidential interval = − 1.193 to − 0.249; P = 0.002) in multivariate analysis. We demonstarted the association between impaired ocular blood flow (parapapillary choroidal vessel density) and autonomic dysfunction (LF/HF ratio). This study could help understand the role of the autonomic dysfunction in pathophysiology of glaucoma progression.

The purpose of this study was to design an animal model mimicking glaucoma with hemodynamic instability and to identify involvement of angiotensin II (AngII) and associated changes of the retina. Systemic hypotension was induced in Sprague–Dawley rats by oral hydrochlorothiazide administration. Rats were sacrificed at 4, 8, and 12-week time points. AngII and receptor levels were examined in the serum and retina. To examine the relationship between glia activation and associated RGC death, biochemical analysis of GFAP, Iba-1, and necroptosis associated factors such as TNFα, receptor-interacting protein (RIP) 1, 3, and inactive caspase 8 were explored. To investigate the difference in RGC death mechanism, JNK inhibitor or RIP3 inhibitor were given intraperitoneally to rats with ocular hypertension and systemic hypotension both to identify the pathway mainly involved. AngII and receptors were increased in the serum and retina of systemic hypotensive rat. At 4, 8, and 12 weeks after hypotension induction, glial activation was increased as indicated by GFAP and Iba-1 staining. TNFα, RIP3 were elevated. and downregulation of inactive caspase 8 was apparent in the retina of hypotensive rat. Electron microscopy revealed that necroptosis of RGC was gradually increased after systemic hypotension. Following intraperitoneal JNK inhibitor or RIP3 inhibitor administration, RGC loss was attenuated in systemic hypotensive rats but not in ocular hypertensive rats. In conclusion, AngII is involved in glial activation and associated RGC necroptosis following systemic hypotension. This pathway represents a novel and distinct cell death mechanism when compared to that involved in elevated intraocular pressure.

Purpose: The purpose of this study was to investigate the ocular and hemodynamic factors contributing to the central visual function in glaucoma patients with myopia. Methods: This study was a prospective observational study, which included 236 eyes of 140 patients with normal-tension glaucoma (NTG), which includes 114 eyes with mild myopia (axial length ≥24 and <26 mm) and 122 eyes with moderate-to-severe myopia (axial length ≥26 mm). Ocular characteristics were axial length and posterior pole profiles, including peripapillary atrophy (PPA) to disc area ratio, disc tilt ratio, disc torsion, and disc-foveal angle. Hemodynamic factors included standard deviation of the mean of qualified normal-to-normal intervals (SDNN) of a heart rate variability (HRV) test and vessel density (VD) parameters from optical coherence tomography angiography (OCTA). The root mean square error was estimated as a measure of the VD fluctuation. Association between ocular characteristics and VD parameters of the OCTA with the central sensitivity of the 10-degree visual field or the presence of central scotoma were analyzed. Results: Deep layer VD of the peripapillary and macular areas showed significant differences between mild and moderate-to-severe myopia (P = 0.034 and P = 0.045, respectively). Structural parameters, especially PPA to disc area ratio, had significant correlation with peripapillary VD parameters in myopic eyes. Lower SDNN value (ß = 0.924, P = 0.011), lower deep VD of the macular area (ß = 0.845, P = 0.001), and greater fluctuation of deep VD in the peripapillary area (ß = 1.517, P = 0.005) were associated with the presence of central scotoma in patients with glaucoma with myopia in multivariate logistic regression analysis. Conclusions: The structural changes by myopia, especially in the peripapillary region, affected VD parameters in myopic eyes. Lower deep VD and greater VD fluctuation in the peripapillary region showed association with central scotoma in patients with glaucoma with myopia, suggesting both structural and vascular changes by myopia may be related to central visual function in glaucoma patients with myopia.