Effects of Acute High-Altitude Exposure on Morphology and Function of Retinal Ganglion Cell in Mice.
Yang Yi, Han Cong, Sun Yi, Zhao Xin, Chen Zhaoqian, Zhao Liangtao, Li Yuting, Zhang Wenfang
AI Summary
Acute high-altitude exposure in mice damaged retinal ganglion cell morphology and function, including RGC loss and reduced electrical responses. This provides insight into high-altitude retinopathy mechanisms and prevention.
Abstract
Purpose
High altitude retinopathy (HAR) is a retinal functional disorder caused by inadequate adaptation after exposure to high altitude. However, the cellular and molecular mechanisms underlying retinal dysfunction remain elusive. Retinal ganglion cell (RGC) injury is the most important pathological basis for most retinal and optic nerve diseases. Studies focusing on RGC injury after high-altitude exposure (HAE) are scanty. Therefore, the present study sought to explore both functional and morphological alterations of RGCs after HAE.
Methods
A mouse model of acute hypobaric hypoxia was established by mimicking the conditions of a high altitude of 5000 m. After HAE for 2, 4, 6, 10, 24, and 72 hours, the functional and morphological alterations of RGCs were assessed using retinal hematoxylin and eosin (H&E) sections, retinal whole mounts, transmission electron microscopy (TEM), and the photopic negative response (PhNR) of the electroretinogram.
Results
Compared with the control group, the thickness of the ganglion cell layer and retinal nerve fiber layer increased significantly, RGC loss remained significant, and the amplitudes of a-wave, b-wave, and PhNR were significantly reduced after HAE. In addition, RGCs and their axons exhibited an abnormal ultrastructure after HAE, including nuclear membrane abnormalities, uneven distribution of chromatin in the nucleus, decreased cytoplasmic electron density, widening and vacuolization of the gap between axons, loosening and disorder of myelin sheath structure, widening of the gap between myelin sheath and axon membrane, decreased axoplasmic density, unclear microtubule and nerve fiber structure, and abnormal mitochondrial structure (mostly swollen, with widened membrane gaps and reduced cristae and vacuolization).
Conclusions
The study findings confirm that the morphology and function of RGCs are damaged after HAE. These findings lay the foundation for further study of the specific molecular mechanisms of HAR and promote the effective prevention.
MeSH Terms
Shields Classification
Key Concepts5
After high-altitude exposure (HAE) for 2, 4, 6, 10, 24, and 72 hours, the thickness of the ganglion cell layer and retinal nerve fiber layer significantly increased in mice compared with the control group.
After high-altitude exposure (HAE) for 2, 4, 6, 10, 24, and 72 hours, significant retinal ganglion cell (RGC) loss was observed in mice compared with the control group.
After high-altitude exposure (HAE) for 2, 4, 6, 10, 24, and 72 hours, the amplitudes of a-wave, b-wave, and photopic negative response (PhNR) were significantly reduced in mice compared with the control group.
After high-altitude exposure (HAE) for 2, 4, 6, 10, 24, and 72 hours, retinal ganglion cells (RGCs) and their axons in mice exhibited abnormal ultrastructure, including nuclear membrane abnormalities, uneven chromatin distribution, decreased cytoplasmic electron density, widening and vacuolization of the gap between axons, loosening and disorder of myelin sheath structure, widening of the gap between myelin sheath and axon membrane, decreased axoplasmic density, unclear microtubule and nerve fiber structure, and abnormal mitochondrial structure (swollen, widened membrane gaps, reduced cristae, and vacuolization).
A mouse model of acute hypobaric hypoxia was established by mimicking the conditions of a high altitude of 5000 m to study the effects of high-altitude exposure (HAE) on retinal ganglion cells (RGCs).
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