scholarly journals The Rodent Model of Nonarteritic Anterior Ischemic Optic Neuropathy (rNAION)

10.3791/54504 ◽  
2016 ◽  
Author(s):  
Yan Guo ◽  
Zara Mehrabian ◽  
Steven L. Bernstein
Keyword(s):  
Optic Neuropathy ◽  
Rodent Model ◽  
Anterior Ischemic Optic Neuropathy ◽  
Ischemic Optic Neuropathy

scholarly journals Protective effects of quercetin in a rodent model of anterior ischemic optic neuropathy (rAION)

2019 ◽  
Author(s):  
Ya-nan Lyu ◽  
Jing-yu Min ◽  
Yuanyuan Gong ◽  
qing Gu ◽  
fang Wei
Keyword(s):  
Intravitreal Injection ◽  
Optic Neuropathy ◽  
Vision Loss ◽  
Ganglion Cells ◽  
Rodent Model ◽  
Anterior Ischemic Optic Neuropathy ◽  
Ischemic Optic Neuropathy ◽  
Protective Effects ◽  
High Power Field ◽  
Optic Nerves

Abstract Background: Anterior ischemic optic neuropathy (AION) is the leading cause of sudden optic nerve-related (ON-related) vision loss in elderly people. However, no considerable treatments are available for the neuroprotection of NAION. The purpose of this study was to detect the effects of intravitreal injection of quercetin (Qcn) in a rodent model of anterior ischemic optic neuropathy (rAION). Methods: The rAION model was established using verteporfin and laser in a photodynamic procedure on the optic discs (ON) of rats. The rats received intravitreal injection of Qcn 2 days before the injury and once/week for 4 weeks after the infarct on optic neuropathy. Flash-visual evoked potential (VEP) were recorded to assess the visual function. TUNEL and retrograde Fluorogold labeling assessed the apoptosis and density of retinal ganglion cells (RGCs). ED-1 and Iba-1 staining of the optic nerves displayed the inflammatory response. Results: At 14 days post-infarct, Qcn treatment significantly reduced the number of apoptotic RGCs, as well as, ED1/Iba-1-positive cells/high power field(HPF) in the ON (p<0.01) as compared to the rAION group. At week 4 after rAION, 28.4% VEP amplitudes were estimated in the treated eyes of the fellow eyes in the rAION group and 64.7% in the rAION+Qcn group (p<0.01). In addition, Qcn saved the RGCs in the central retinas as compared to those of the rAION group (1967.5±162.1 and 2868±325.3 mm2, respectively (p<0.01), and the corresponding densities were 1654.8±104.8 and 2208±272.9 mm2 in the mid-peripheral retinas, respectively (p<0.01). Conclusion: The intravitreal injection of Qcn could protect the RGCs from injury in the rAION animal model, as demonstrated anatomically by RGC density and functionally by F-VEP. Moreover, Qcn might exert an anti-apoptosis role in the survival of RGCs and anti-inflammatory in the optic nerves.

scholarly journals Optic Nerve Inflammation and Demyelination in a Rodent Model of Nonarteritic Anterior Ischemic Optic Neuropathy

2013 ◽  
Vol 54 (13) ◽  
pp. 7952 ◽  
Author(s):  
Bernard J. Slater ◽  
Fernandino L. Vilson ◽  
Yan Guo ◽  
Daniel Weinreich ◽  
Shelly Hwang ◽  
...  
Keyword(s):  
Optic Nerve ◽  
Optic Neuropathy ◽  
Rodent Model ◽  
Anterior Ischemic Optic Neuropathy ◽  
Ischemic Optic Neuropathy

scholarly journals Protective Effects of Intravitreal Injection of the Rho-Kinase Inhibitor Y-27632 in a Rodent Model of Nonarteritic Anterior Ischemic Optic Neuropathy (rAION)

2020 ◽  
Vol 2020 ◽  
pp. 1-9
Author(s):  
Zuohuizi Yi ◽  
Liao Chen ◽  
Xiaoling Wang ◽  
Changzheng Chen ◽  
Yiqiao Xing
Keyword(s):  
Intravitreal Injection ◽  
Optic Neuropathy ◽  
Visual Function ◽  
Kinase Inhibitor ◽  
Rho Kinase ◽  
Rodent Model ◽  
Anterior Ischemic Optic Neuropathy ◽  
Ischemic Optic Neuropathy ◽  
Neuroprotective Effects ◽  
Rho Kinase Inhibitor

Purpose. We sought to explore the effects of intravitreal injection of the Rho-kinase inhibitor Y-27632 in a rodent model of nonarteritic anterior ischemic optic neuropathy (rAION). Methods. The rAION model was established by using laser-induced photoactivation of intravenously administered Rose Bengal in rats. The rats received intravitreal injections of Y-27632 or PBS 1, 3, and 6 days after rAION induction. Optical coherence tomography (OCT) was performed at 2 days and 4 weeks after induction. Visual evoked potential (VEP) was used to evaluate the visual function at 4 weeks. Brn3a immunofluorescence staining of surviving RGCs and apoptosis assays of RGCs were performed at 4 weeks. Results. Optic nerve head (ONH) width was significantly reduced in the Y-27632 group compared with that in the PBS group at 2 days after induction (p<0.05). At 4 weeks, the P1 amplitude of flash-VEP (FVEP) in the Y-27632 group was significantly higher than that of the PBS group (p<0.05). The RGC densities in the central and midperipheral retinas in the Y-27632 group were significantly higher than those in the PBS group (p<0.05). Furthermore, there was a significant decrease in apoptotic RGCs in the Y-27632 group than in the PBS group (p<0.05). Conclusions. Intravitreal injection of Y-27632 had neuroprotective effects on ONH edema, RGC survival, and visual function preservation in rAION.

Functional and Cellular Responses in a Novel Rodent Model of Anterior Ischemic Optic Neuropathy

2003 ◽  
Vol 44 (10) ◽  
pp. 4153 ◽  
Author(s):  
Steven L. Bernstein ◽  
Yan Guo ◽  
Shalom E. Kelman ◽  
Robert W. Flower ◽  
Mary A. Johnson
Keyword(s):  
Optic Neuropathy ◽  
Cellular Responses ◽  
Rodent Model ◽  
Anterior Ischemic Optic Neuropathy ◽  
Ischemic Optic Neuropathy

scholarly journals Biomarkers of lesion severity in a rodent model of nonarteritic anterior ischemic optic neuropathy (rNAION)

2020 ◽  
Author(s):  
Yan Guo ◽  
Zara Mehrabian ◽  
Mary A. Johnson ◽  
Neil R. Miller ◽  
Amanda D. Henderson ◽  
...  
Keyword(s):  
Optic Neuropathy ◽  
Rodent Model ◽  
Anterior Ischemic Optic Neuropathy ◽  
Laser Exposure ◽  
Ischemic Optic Neuropathy ◽  
Sprague Dawley ◽  
Relative Level ◽  
Cross Sectional ◽  
Post Induction ◽  
Lesion Severity

AbstractThe rodent model of nonarteritic anterior ischemic optic neuropathy (rNAION) is similar in many of its pathophysiological responses to clinical NAION. However, little is known of the parameters associated with rNAION induction severity and if pre- or early post-induction biomarkers can be identified that enable prediction of lesion severity and ultimate loss of retinal ganglion cells (RGCs). Adult male Sprague-Dawley outbred rats were evaluated for various parameters including physiological characteristics (heart rate, respiratory rate, temperature, hematocrit), optic nerve head (ONH) appearance, pre- and post-induction mean diameter, and intravenous fluorescein and indocyanine green angiographic patterns of vascular leakage at 5 hours post-induction, performed using a spectral domain-optical coherence tomography (SD-OCT) instrument. These parameters were correlated with ultimate RGC loss by Brn3a (+) immunohistology. RGC loss also was correlated with the relative level of laser exposure. The severity of ONH edema 2d, but not 5hr, post induction was most closely associated with the degree of RGC loss, revealing a threshold effect, and consistent with a compartment syndrome where a minimum level of capillary compression within a tight space is responsible for damage. RGC loss increased dramatically as the degree of laser exposure increased. Neither physiological parameters nor the degree of capillary leakage 5hr post induction were informative as to the ultimate degree of RGC loss. Similar to human NAION, the rNAION model exhibits marked variability in lesion severity. Unlike clinical NAION, pre-induction ONH diameter likely does not contribute to ultimate lesion severity; however, cross-sectional ONH edema can be used as a biomarker 1-2d post-induction to determine randomization of subjects prior to inclusion in specific neuroprotection or neuroregeneration studies.

scholarly journals Biomarkers of lesion severity in a rodent model of nonarteritic anterior ischemic optic neuropathy (rNAION)

PLoS ONE ◽  
2021 ◽  
Vol 16 (3) ◽  
pp. e0243186
Author(s):  
Yan Guo ◽  
Zara Mehrabian ◽  
Mary A. Johnson ◽  
Neil R. Miller ◽  
Amanda D. Henderson ◽  
...  
Keyword(s):  
Optic Neuropathy ◽  
Rodent Model ◽  
Anterior Ischemic Optic Neuropathy ◽  
Laser Exposure ◽  
Ischemic Optic Neuropathy ◽  
Sprague Dawley ◽  
Relative Level ◽  
Cross Sectional ◽  
Post Induction ◽  
Lesion Severity

The rodent model of nonarteritic anterior ischemic optic neuropathy (rNAION) is similar in many of its pathophysiological responses to clinical NAION. Like human NAION, there is significant variability in the severity of the lesion produced, and little is known of the parameters associated with rNAION induction severity or if pre- or early post-induction biomarkers can be identified that enable prediction of lesion severity and ultimate loss of retinal ganglion cells (RGCs). Adult male Sprague-Dawley outbred rats were evaluated for various parameters including physiological characteristics (heart rate, respiratory rate, temperature, hematocrit [Hct]), optic nerve head (ONH) appearance, pre- and post-induction mean diameter, and intravenous fluorescein and indocyanine green angiographic patterns of vascular leakage at 5 hours post-induction, performed using a spectral domain-optical coherence tomography (SD-OCT) instrument. Early changes were correlated with ultimate RGC loss by Brn3a (+) immunohistology. RGC loss also was correlated with the relative level of laser exposure. The severity of ONH edema 2d, but not 5hr, post induction was most closely associated with the degree of RGC loss, revealing a threshold effect, and consistent with a compartment syndrome where a minimum level of capillary compression within a tight space is responsible for damage. RGC loss increased dramatically as the degree of laser exposure increased. Neither physiological parameters nor the degree of capillary leakage 5hr post induction were informative as to the ultimate degree of RGC loss. Similar to human NAION, the rNAION model exhibits marked variability in lesion severity. Unlike clinical NAION, pre-induction ONH diameter likely does not contribute to ultimate lesion severity; however, cross-sectional ONH edema can be used as a biomarker 2d post-induction to determine randomization of subjects prior to inclusion in specific neuroprotection or neuroregeneration studies.

Sign in / Sign up

Export Citation Format

Share Document