A New Optokinetic Testing Method to Measure Rat Vision

Ahmed, Faizah; Nair, Deepthi S. Rajendran; Thomas, Biju

doi:10.3791/63357

Cited by 2 publications

(1 citation statement)

References 21 publications

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“…Experimental methods to measure rodent vision exist, such as measurements of optokinetic nystagmus and optomotor response/reflex. [ 13 , 14 ] While these methods offer valuable insights into certain aspects of vision, they lack direct assessment of functional vision because they only measure the reflexive eye movements in response to visual stimuli and not the ability of mice to navigate using vision. The Morris water maze has been modified by several investigators to assess visually guided navigation.…”

Section: Introductionmentioning

confidence: 99%

A visually guided swim assay for mouse models of human retinal disease recapitulates the multi-luminance mobility test in humans

Hassan,

Hsu,

Mayer

et al. 2023

Saudi Journal of Ophthalmology

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PURPOSE: The purpose of this study was to develop a visually guided swim assay (VGSA) for measuring vision in mouse retinal disease models comparable to the multi-luminance mobility test (MLMT) utilized in human clinical trials. METHODS: Three mouse retinal disease models were studied: Bardet–Biedl syndrome type 1 (Bbs1M390R/M390R ), n = 5; Bardet–Biedl syndrome type 10 (Bbs10−/− ), n = 11; and X linked retinoschisis (retinoschisin knockout; Rs1-KO), n = 5. Controls were normally-sighted mice, n = 10. Eyeless Pax6Sey-Dey mice, n = 4, were used to determine the performance of animals without vision in VGSA. RESULTS: Eyeless Pax6Sey-Dey mice had a VGSA time-to-platform (TTP) 7X longer than normally-sighted controls (P < 0.0001). Controls demonstrated no difference in their TTP in both lighting conditions; the same was true for Pax6Sey-Dey . At 4–6 M, Rs1-KO and Bbs10−/− had longer TTP in the dark than controls (P = 0.0156 and P = 1.23 × 10−8, respectively). At 9–11 M, both BBS models had longer TTP than controls in light and dark with times similar to Pax6Sey-Dey (P < 0.0001), demonstrating progressive vision loss in BBS models, but not in controls nor in Rs1-KO. At 1 M, Bbs10−/− ERG light-adapted (cone) amplitudes were nonrecordable, resulting in a floor effect. VGSA did not reach a floor until 9–11 M. ERG combined rod/cone b-wave amplitudes were nonrecordable in all three mutant groups at 9–11 M, but VGSA still showed differences in visual function. ERG values correlate non-linearly with VGSA, and VGSA measured the continual decline of vision. CONCLUSION: ERG is no longer a useful endpoint once the nonrecordable level is reached. VGSA differentiates between different levels of vision, different ages, and different disease models even after ERG is nonrecordable, similar to the MLMT in humans.

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Section: Introductionmentioning

confidence: 99%

A visually guided swim assay for mouse models of human retinal disease recapitulates the multi-luminance mobility test in humans

Hassan,

Hsu,

Mayer

et al. 2023

Saudi Journal of Ophthalmology

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Effect of recurrent severe insulin-induced hypoglycemia on the cognitive function and brain oxidative status in the rats

Nikpendar,

Javanbakht,

Moosavian

et al. 2024

Diabetol Metab Syndr

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Background Episodes of recurrent or severe hypoglycemia can occur in patients with diabetes mellitus, insulinoma, neonatal hypoglycemia, and medication errors. However, little is known about the short-term and long-term effects of repeated episodes of acute severe hypoglycemia on the brain, particularly in relation to hippocampal damage and cognitive dysfunction. Methods Thirty-six wistar rats were randomly assigned to either the experimental or control group. The rats were exposed to severe hypoglycemia, and assessments were conducted to evaluate oxidative stress in brain tissue, cognitive function using the Morris water maze test, as well as histopathology and immunohistochemistry studies. The clinical and histopathological evaluations were conducted in the short-term and long-term. Results The mortality rate attributed to hypoglycemia was 34%, occurring either during hypoglycemia or within 24 h after induction. Out of the 14 rats monitored for 7 to 90 days following severe/recurrent hypoglycemia, all exhibited clinical symptoms, which mostly resolved within three days after the last hypoglycemic episode, except for three rats. Despite the decrease in catalase activity in the brain, the total antioxidant capacity following severe insulin-induced hypoglycemia increased. The histopathology findings revealed that the severity of the hippocampal damage was higher compared to the brain cortex 90 days after hypoglycemia. Memory impairments with neuron loss particularly pronounced in the dentate gyrus region of the hippocampus were observed in the rats with severe hypoglycemia. Additionally, there was an increase in reactive astrocytes indicated by GFAP immunoreactivity in the brain cortex and hippocampus. Conclusion Recurrent episodes of severe hypoglycemia can lead to high mortality rates, memory impairments, and severe histopathological changes in the brain. While many histopathological and clinical changes improved after three months, it seems that the vulnerability of the hippocampus and the development of sustained changes in the hippocampus were greater and more severe compared to the brain cortex following severe and recurrent hypoglycemia. Furthermore, it does not appear that oxidative stress plays a central role in neuronal damage following severe insulin-induced hypoglycemia. Further research is necessary to assess the consequences of repeated hypoglycemic episodes on sustained damage across various brain regions.

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A New Optokinetic Testing Method to Measure Rat Vision

Cited by 2 publications

References 21 publications

A visually guided swim assay for mouse models of human retinal disease recapitulates the multi-luminance mobility test in humans

A visually guided swim assay for mouse models of human retinal disease recapitulates the multi-luminance mobility test in humans

Effect of recurrent severe insulin-induced hypoglycemia on the cognitive function and brain oxidative status in the rats

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