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A microgravity environment has been shown to cause ocular damage and affect visual acuity, but the underlying mechanisms remain unclear. Therefore, we established an animal model of weightlessness via tail suspension to examine the pathological changes and molecular mechanisms of retinal damage under microgravity. After 4 weeks of tail suspension, there were no notable alterations in retinal function and morphology, while after 8 weeks of tail suspension, significant reductions in retinal function were observed, and the outer nuclear layer was thinner, with abundant apoptotic cells. To investigate the mechanism underlying the degenerative changes that occurred in the outer nuclear layer of the retina, proteomics was used to analyze differentially expressed proteins in rat retinas after 8 weeks of tail suspension. The results showed that the expression levels of fibroblast growth factor 2 (also known as basic fibroblast growth factor) and glial fibrillary acidic protein, which are closely related to Müller cell activation, were significantly upregulated. In addition, Müller cell regeneration and Müller cell gliosis were observed after 4 and 8 weeks, respectively, of simulated weightlessness. These findings indicate that Müller cells play an important regulatory role in retinal outer nuclear layer degeneration during weightlessness.

The article discusses the study which investigates the link between pupil area differences, heart rate inconsistency and fatigue, due to alcohol consumption. The study involved 16 young male volunteers, in whom it assessed drinking volume and motion of pupils. It also used methods such as electrocardiography, analysis of variance (ANOVA) and multiple comparison tests. Results show that fatigue level of an individual may be verified by relevant changes in pupil region and heart beat.

The article discusses a study that explored Fos protein expression differences of vestibular-related nucleus populations in a mouse with rapid retinal degeneration and normal wild-type Kunming mice after rotary motion. Various studies showed that visual and vestibular information conflicts in the central nervous system are responsible for inducing motion sickness and spatial disorientation. The results revealed that visual information affects neuronal activation in the prepositus hypoglossal necleus and the Kooy cap of the inferior olive medial nucleus.