A 3D-Printed and Freely Available Device to Measure the Zebrafish Optokinetic Response Before and After Injury.

Zebrafish eyes are anatomically similar to humans and have a higher percentage of cone photoreceptors more akin to humans than most rodent models, making them a beneficial model organism for studying vision. However, zebrafish are different in that they can regenerate their optic nerve after injury, which most other animals cannot. Vision in zebrafish and many other vertebrate animals, including humans, can be accessed using the optokinetic response (OKR), which is an innate eye movement that occurs when tracking an object. Because fish cannot use an eye chart, we utilize the OKR that is present in virtually all vertebrates to determine if a zebrafish has vision. To this end, we have developed an inexpensive OKR setup that uses 3D-printed and off-the-shelf parts. This setup has been designed and used by undergraduate researchers and is also scalable to a classroom laboratory setup. We demonstrate that this setup is fully functional for assessing the OKR, and we use it to illustrate the return of the OKR following optic nerve injury in adult zebrafish.

Interleukin-4 protects retinal ganglion cells and promotes axon regeneration.

BACKGROUND: The preservation of retinal ganglion cells (RGCs) and the facilitation of axon regeneration are crucial considerations in the management of various vision-threatening disorders. Therefore, we investigate the efficacy of interleukin-4 (IL-4), a potential therapeutic agent, in promoting neuroprotection and axon regeneration of retinal ganglion cells (RGCs) as identified through whole transcriptome sequencing in an in vitro axon growth model. METHODS: A low concentration of staurosporine (STS) was employed to induce in vitro axon growth. Whole transcriptome sequencing was utilized to identify key target factors involved in the molecular mechanism underlying axon growth. The efficacy of recombinant IL-4 protein on promoting RGC axon growth was validated through in vitro experiments. The protective effect of recombinant IL-4 protein on somas of RGCs was assessed using RBPMS-specific immunofluorescent staining in mouse models with optic nerve crush (ONC) and N-methyl-D-aspartic acid (NMDA) injury. The protective effect on RGC axons was evaluated by anterograde labeling of cholera toxin subunit B (CTB), while the promotion of RGC axon regeneration was assessed through both anterograde labeling of CTB and immunofluorescent staining for growth associated protein-43 (GAP43). RESULTS: Whole-transcriptome sequencing of staurosporine-treated 661 W cells revealed a significant upregulation in intracellular IL-4 transcription levels during the process of axon regeneration. In vitro experiments demonstrated that recombinant IL-4 protein effectively stimulated axon outgrowth. Subsequent immunostaining with RBPMS revealed a significantly higher survival rate of RGCs in the rIL-4 group compared to the vehicle group in both NMDA and ONC injury models. Axonal tracing with CTB confirmed that recombinant IL-4 protein preserved long-distance projection of RGC axons, and there was a notably higher number of surviving axons in the rIL-4 group compared to the vehicle group following NMDA-induced injury. Moreover, intravitreal delivery of recombinant IL-4 protein substantially facilitated RGC axon regeneration after ONC injury. CONCLUSION: The recombinant IL-4 protein exhibits the potential to enhance the survival rate of RGCs, protect RGC axons against NMDA-induced injury, and facilitate axon regeneration following ONC. This study provides an experimental foundation for further investigation and development of therapeutic agents aimed at protecting the optic nerve and promoting axon regeneration.

Assessing Stress Induced by Fluid Shifts and Reduced Cerebral Clearance during Robotic-Assisted Laparoscopic Radical Prostatectomy under Trendelenburg Positioning (UroTreND Study).

In addition to general anesthesia and mechanical ventilation, robotic-assisted laparoscopic radical prostatectomy (RALP) necessitates maintaining a capnoperitoneum and placing the patient in a pronounced downward tilt (Trendelenburg position). While the effects of the resulting fluid shift on the cardiovascular system seem to be modest and well tolerated, the effects on the brain and the blood-brain barrier have not been thoroughly investigated. Previous studies indicated that select patients showed an increase in the optic nerve sheath diameter (ONSD), detected by ultrasound during RALP, which suggests an elevation in intracranial pressure. We hypothesize that the intraoperative fluid shift results in endothelial dysfunction and reduced cerebral clearance, potentially leading to transient neuronal damage. This prospective, monocentric, non-randomized, controlled clinical trial will compare RALP to conventional open radical prostatectomy (control group) in a total of 50 subjects. The primary endpoint will be the perioperative concentration of neurofilament light chain (NfL) in blood using single-molecule array (SiMoA) as a measure for neuronal damage. As secondary endpoints, various other markers for endothelial function, inflammation, and neuronal damage as well as the ONSD will be assessed. Perioperative stress will be evaluated by questionnaires and stress hormone levels in saliva samples. Furthermore, the subjects will participate in functional tests to evaluate neurocognitive function. Each subject will be followed up until discharge. Conclusion: This trial aims to expand current knowledge as well as to develop strategies for improved monitoring and higher safety of patients undergoing RALP. The trial was registered with the German Clinical Trials Register DRKS00031041 on 11 January 2023.

NFATc4 Knockout Promotes Neuroprotection and Retinal Ganglion Cell Regeneration After Optic Nerve Injury.

Retinal ganglion cells (RGCs), neurons transmitting visual information via the optic nerve, fail to regenerate their axons after injury. The progressive loss of RGC function underlies the pathophysiology of glaucoma and other optic neuropathies, often leading to irreversible blindness. Therefore, there is an urgent need to identify the regulators of RGC survival and the regenerative program. In this study, we investigated the role of the family of transcription factors known as nuclear factor of activated T cells (NFAT), which are expressed in the retina; however, their role in RGC survival after injury is unknown. Using the optic nerve crush (ONC) model, widely employed to study optic neuropathies and central nervous system axon injury, we found that NFATc4 is specifically but transiently up-regulated in response to mechanical injury. In the injured retina, NFATc4 immunolocalized primarily to the ganglionic cell layer. Utilizing NFATc4-/- and NFATc3-/- mice, we demonstrated that NFATc4, but not NFATc3, knockout increased RGC survival, improved retina function, and delayed axonal degeneration. Microarray screening data, along with decreased immunostaining of cleaved caspase-3, revealed that NFATc4 knockout was protective against ONC-induced degeneration by suppressing pro-apoptotic signaling. Finally, we used lentiviral-mediated NFATc4 delivery to the retina of NFATc4-/- mice and reversed the pro-survival effect of NFATc4 knockout, conclusively linking the enhanced survival of injured RGCs to NFATc4-dependent mechanisms. In summary, this study is the first to demonstrate that NFATc4 knockout may confer transient RGC neuroprotection and decelerate axonal degeneration after injury, providing a potent therapeutic strategy for optic neuropathies.

Mesenchymal stem cells for repairing glaucomatous optic nerve.

Glaucoma is a common and complex neurodegenerative disease characterized by progressive loss of retinal ganglion cells (RGCs) and axons. Currently, there is no effective method to address the cause of RGCs degeneration. However, studies on neuroprotective strategies for optic neuropathy have increased in recent years. Cell replacement and neuroprotection are major strategies for treating glaucoma and optic neuropathy. Regenerative medicine research into the repair of optic nerve damage using stem cells has received considerable attention. Stem cells possess the potential for multidirectional differentiation abilities and are capable of producing RGC-friendly microenvironments through paracrine effects. This article reviews a thorough researches of recent advances and approaches in stem cell repair of optic nerve injury, raising the controversies and unresolved issues surrounding the future of stem cells.

Regulation of Diseases-Associated Microglia in the Optic Nerve by Lipoxin B4 and Ocular Hypertension.

Background: The resident astrocyte-retinal ganglion cell (RGC) lipoxin circuit is impaired during retinal stress, which includes ocular hypertension-induced neuropathy. Lipoxin B4 produced by homeostatic astrocytes directly acts on RGCs to increase survival and function in ocular hypertension-induced neuropathy. RGC death in the retina and axonal degeneration in the optic nerve are driven by the complex interactions between microglia and macroglia. Whether LXB4 neuroprotective actions include regulation of other cell types in the retina and/or optic nerve is an important knowledge gap. Methods: Cellular targets and signaling of LXB4 in the retina were defined by single-cell RNA sequencing. Retinal neurodegeneration was induced by injecting silicone oil into the anterior chamber of the mouse eyes, which induced sustained and stable ocular hypertension. Morphological characterization of microglia populations in the retina and optic nerve was established by MorphOMICs and pseudotime trajectory analyses. The pathways and mechanisms of action of LXB4 in the optic nerve were investigated using bulk RNA sequencing. Transcriptomics data was validated by qPCR and immunohistochemistry. Differences between experimental groups was assessed by Student's t-test and one-way ANOVA. Results: Single-cell transcriptomics identified microglia as a primary target for LXB4 in the healthy retina. LXB4 downregulated genes that drive microglia environmental sensing and reactivity responses. Analysis of microglial function revealed that ocular hypertension induced distinct, temporally defined, and dynamic phenotypes in the retina and, unexpectedly, in the distal myelinated optic nerve. Microglial expression of CD74, a marker of disease-associated microglia in the brain, was only induced in a unique population of optic nerve microglia, but not in the retina. Genetic deletion of lipoxin formation correlated with the presence of a CD74 optic nerve microglia population in normotensive eyes, while LXB4 treatment during ocular hypertension shifted optic nerve microglia toward a homeostatic morphology and non-reactive state and downregulated the expression of CD74. Furthermore, we identified a correlation between CD74 and phospho-phosphoinositide 3-kinases (p-PI3K) expression levels in the optic nerve, which was reduced by LXB4 treatment. Conclusion: We identified early and dynamic changes in the microglia functional phenotype, reactivity, and induction of a unique CD74 microglia population in the distal optic nerve as key features of ocular hypertension-induced neurodegeneration. Our findings establish microglia regulation as a novel LXB4 target in the retina and optic nerve. LXB4 maintenance of a homeostatic optic nerve microglia phenotype and inhibition of a disease-associated phenotype are potential neuroprotective mechanisms for the resident LXB4 pathway.

Improved optic nerve visualization and treatment planning through a dedicated optic nerve MRI protocol.

OBJECTIVE: This study describes an innovative optic nerve MRI protocol for better delineating optic nerve anatomy from neighboring pathology. METHODS: Twenty-two patients undergoing MRI examination of the optic nerve with the dedicated protocol were identified and included for analysis of imaging, surgical strategy, and outcomes. T2-weighted and fat-suppressed T1-weighted gadolinium-enhanced images were acquired perpendicular and parallel to the long axis of the optic nerve to achieve en face and in-line views along the course of the nerve. RESULTS: Dedicated optic nerve MRI sequences provided enhanced visualization of the nerve, CSF within the nerve sheath, and local pathology. Optic nerve sequences leveraged the "CSF ring" within the optic nerve sheath to create contrast between pathology and normal tissue, highlighting areas of compression. Tumor was readily tracked along the longitudinal axis of the nerve by images obtained parallel to the nerve. The findings augmented treatment planning. CONCLUSIONS: The authors present a dedicated optic nerve MRI protocol that is simple to use and affords improved cross-sectional and longitudinal visualization of the nerve, surrounding CSF, and pathology. This improved visualization enhances radiological evaluation and treatment planning for optic nerve lesions.

Normative measurements of orbital structures on magnetic resonance images; a cross-sectional study with mini review of the literature.

PURPOSE: Awareness of normative values of extra orbital structures would provide useful information to interpret the radiological images better and use them for diagnostic purposes. This study aimed to reveal the average values of major extraocular structures measured on magnetic resonance images. METHODS: In this retrospective cross-sectional study, magnetic resonance (MR) images of 256 orbits of 128 patients were re-interpreted regarding the measurements of major orbital structures. Extraocular muscles, superior ophthalmic vein, and optic nerve-sheath complex were measured on orbital MR images of these patients. The data distributions were presented by box-plot analyses for each parameter, and the measurement results were analyzed regarding gender and age groups. RESULTS: Lateral rectus muscle thickness (LR), inferior rectus muscle thickness (IR), globe position (GP), and interzygomatic line (IZL) values were higher in the male group than in the female group (p values were < 0.001, 0.003, 0.020, and < 0.001 respectively). LR, the thickness of the superior group muscles (SUP GR), IR, superior oblique muscle thickness (SOBL), and the thickness of optic nerve-sheath complex (ON) values indicated a significant relationship between age groups. There was a significant, positive, and low-level correlation between age and LR, SUP GR, and IR values (p values were < 0.001, 0.001, and < 0.001, respectively). CONCLUSION: This study provides quantitative data on normative values of orbital structures with gender and age group comparisons. Clinicians or surgeons can easily use the measured values to gather diagnostic information from the orbital region.

Neurodevelopmental disorder in a patient with HMBS and SCN3A variants-A possibly blended phenotype further delineating autosomal recessive HMBS related disease.

Monoallelic pathogenic HMBS variants are a well-established cause of acute intermittent porphyria (AIP), whereas biallelic pathogenic variants may cause HMBS-related leukoencephalopathy which remains a poorly characterized disorder. We describe an 8-year-old girl with hypotonia, hearing impairment, horizontal nystagmus, bilateral strabismus, impaired visual acuity, and optic nerve atrophy. She had no epilepsy but sleep electroencephalogram showed paroxysmal changes in the right hemisphere with secondary generalizations. Brain magnetic resonance imaging was unremarkable apart from a few small white matter hyperintensities. Exome sequencing (ES) initially prioritized a SCN3A c.3822G>A de novo variant whose sole causative role was eventually questioned as not fully compatible with symptoms. ES reanalysis revealed a homozygous c.674G>A HMBS variant. In the monoallelic form this variant is a known cause of AIP, whereas in trans with another HMBS pathogenic variant it was associated with the HMBS-related leukoencephalopathy in four individuals. Despite lack of signs/symptoms of porphyria, literature analysis suggested that HMBS c.674G>A likely contributed to the disease either as the sole cause or together with SCN3A c.3822G>A as a part of blended phenotype. Our report adds to the relatively small number of described cases of HMBS-related leukoencephalopathy and emphasizes that autosomal recessive form of HMBS disease can be present in the absence of porphyria symptoms.

Surgical Outcome in Patients with Traumatic and Atraumatic Optic Neuropathy Following Endoscopic Optic Nerve Decompression.

Endoscopic optic nerve decompression is a highly effective and reliable approach for patients with select cases of optic neuropathy. It reduces the hydrostatic pressure and helps in relieving the compressive forces within the intracanalicular portion of the optic nerve consequently preserving and arresting the deterioration of vision. The advantages of the endoscopic approach over other procedures include preservation of olfaction, quick recovery, lack of external scars and less morbidity. The objective of the study is to assess the surgical outcome of endoscopic optic nerve decompression in patients with traumatic and atraumatic optic neuropathy. The case records of consequent patients attending ENT department with defective vision due to traumatic and atraumatic causes were reviewed. The outcome was measured in terms of improvement in visual acuity by log MAR scale. Among the 14 patients studied, 57% were females and the median age of presentation was 33 years. As compared to preoperative baseline visual acuity, the overall improvement was achieved in 11 patients, with an effective rate of 78.5% postoperatively. Patients presenting with no light perception and residual vision had significant improvement in visual acuity after surgery. Trans-nasal endoscopic surgery helps in decompressing the optic nerve with proper exposure of the orbital apex and optic canal without any intracranial or intra-orbital complications. Further, being a minimally invasive procedure has great advantage in cases of optic neuropathy.

Optic Nerve Metastasis in Lung Adenocarcinoma.

In this article, we report a rare case of an optic nerve metastasis secondary to lung adenocarcinoma. The ocular manifestation was the first clinical sign of the disease, and further investigation led to the diagnosis of the underlying malignancy. A 59-year-old woman presented with progressive blurring of vision in the right eye for the past month. She had been having headaches for the past two weeks and left upper limb weakness for one day. She also had loss of appetite and weight for the past few months. She looked lethargic. On presentation, her bilateral eye vision was 6/18. Both anterior segments were unremarkable. Fundoscopy showed a normal optic disc in both eyes. A nervous system examination showed mild motor sensory impairment over the left upper and lower limbs and also impairment of cranial nerves V and VII. Brain computed tomography was conducted and revealed soft tissue lesions at the lateral aspect of the optic nerve and multiple recent cerebral infarcts. Brain and orbital magnetic resonance imaging showed a metastasis intraconal lesion at the right intraorbital segment of the optic nerve. CT thorax, abdomen, and pelvis were done. The finding revealed carcinoma of the left lung with distant metastasis. The patient's general condition deteriorated in less than two weeks. The family refused further intervention. The patient died three months after the initial presentation.

Severe Visual Impairment Following CAR T-Cell Therapy in Two Individuals with Malignant Optic Nerve Infiltration.

We report two patients who displayed evidence of localized ocular inflammation after CAR T-cell infusion. To manage the resulting severe visual impairment, systemic corticosteroids were administered to both patients. This treatment led to a reduction in local inflammation and restored vision in one of the patients.

Peripapillary hyperreflective ovoid mass-like structures: multimodal imaging and associated diseases.

Growing evidence has demonstrated that peripapillary hyperreflective ovoid mass-like structures (PHOMS) are novel structures rather than a subtype of optic disc drusen. They correspond to the laterally bulging herniation of optic nerve fibers and are believed to be the marker of axoplasmic stasis. PHOMS present in a broad spectrum of diseases, including optic disc drusen, tilted disc syndrome, papilloedema, multiple sclerosis, non-arteritic anterior ischemic optic neuropathy, optic neuritis, Leber hereditary optic neuropathy, and so on. We focus on the multimodal imaging features, pathophysiological mechanisms of PHOMS, and their association with multiple diseases and healthy people in this review to deepen the ophthalmologists' understanding of PHOMS. Additionally, we provide some new directions for future research.

Effect of Target Temperature Management on Optic Nerve Sheath Diameter in Post-Cardiac Arrest Patients.

Target Temperature Management (TTM) is a procedure used in post-cardiac arrest (CA) patients to reduce mortality and morbidity. The goal of this study was to investigate the link between intracranial pressure (ICP) and optic nerve sheath diameter (ONSD) in this patient group, which has a high mortality rate, despite TTM, and to see if ONSD may be used to predict mortality. The research was designed to be a retrospective observational study. The study comprised patients who were followed up on in a tertiary intensive care unit, had post-CA TTM, and had brain computed tomography (BCT) before and 0-6 hours after TTM. ONSD measurements were acquired from patients' BCT images recorded before and after TTM. The difference in pre-TTM ONSD and post-TTM ONSD measurements in all post-CA patients, as well as the difference in pre-TTM ONSD and post-TTM ONSD measurements in surviving and deceased patients, was compared. The study involved 33 participants. The patients' average age was 60.58-12.39 years, and 75.8% were male. Around 51.5% of the patients died. When the pre-TTM and post-TTM ONSDs of all patients were compared, there was no statistically significant difference (p = 0.856). When the percentage change (Δ) values between the post-TTM ONSD and pre-TTM ONSD and post-TTM ONSD measures of the surviving patients and the deceased patients were compared, a difference was observed (p < 0.01). Increased ICP in post-CA patients is a significant clinical issue associated with mortality and poor neurological prognosis. ONSD measurement may be useful in monitoring ICP, which may rise, despite TTM, and higher ONSD measurements may be used as an indicator for mortality in post-CA patients, who have received TTM.

Optic disc morphology and interocular symmetry in children.

PURPOSE: The purpose of the study was to obtain a pediatric reference database for optic disc parameters and interocular symmetry. To ascertain factors that modify these parameters (age, spherical equivalent [SE], and sex). METHODS: This was a cross-sectional study. 90 patients aged 5-17 years fulfilled all the inclusion criteria. After a full examination including cycloplegic refraction, all patients underwent optical coherence tomography (OCT) of the papilla using the three-dimensional (3D) scan protocol of the Topcon 3D 2000 OCT device. We provide reference values for optic disc parameters in the pediatric population. We also retrieved interocular symmetry reference values for these parameters. RESULTS: The multivariate regression analysis did not reveal variations in any of the optic disc parameters associated with age, sex, or SE (all P ≥ 0.126). The 95th percentile limit for absolute interocular differences for the cup-to-disc area ratio was 0.24. The multivariate regression analysis revealed the absence of a correlation between asymmetry of the optic disc parameters and age, sex, and the interocular difference in SE (all P ≥ 0.105). CONCLUSION: Pediatric reference databases for optic disc parameters and ranges of normality for interocular symmetry provide key diagnostic support in diseases that affect the optic nerve.

Effect of different positive end expiratory pressure levels on optic nerve sheath diameter in patients with or without midline shift who are undergoing supratentorial craniotomy.

PURPOSE: In general, high levels of PEEP application is avoided in patients undergoing craniotomy to prevent a rise in ICP. But that approach would increase the risk of secondary brain injury especially in hypoxemic patients. Because the optic nerve sheath is distensible, a rise in ICP is associated with an increase in the optic nerve sheath diameter (ONSD). The cutoff value for elevated ICP assessed by ONSD is between 5.6 and 6.3 mm. We aimed to evaluate the effect of different PEEP levels on ONSD and compare the effect of different PEEP levels in patients with and without intracranial midline shift. METHODS: This prospective observational study was performed in aged 18-70 years, ASA I-III, 80 patients who were undergoing supratentorial craniotomy. After the induction of general anesthesia, the ONSD's were measured by the linear transducer from 3 mm below the globe at PEEP values of 0-5-10 cmH2O. The ONSD were compered between patients with (n = 7) and without midline shift (n = 73) at different PEEP values. RESULTS: The increases in ONSD due to increase in PEEP level were determined (p < 0.001). No difference was found in the comparison of ONSD between patients with and without midline shift in different PEEP values (p = 0.329, 0.535, 0.410 respectively). But application of 10 cmH2O PEEP in patients with a midline shift increased the mean ONSD value to 5.73 mm. This value is roughly 0.1 mm higher than the lower limit of the ONSD cutoff value. CONCLUSIONS: The ONSD in adults undergoing supratentorial tumor craniotomy, PEEP values up to 5 cmH2O, appears not to be associated with an ICP increase; however, the ONSD exceeded the cutoff for increased ICP when a PEEP of 10 cmH2O was applied in patients with midline shift.

Dysregulation of neuroprotective lipoxin pathway in astrocytes in response to cytokines and ocular hypertension​.

Glaucoma leads to vision loss due to retinal ganglion cell death. Astrocyte reactivity contributes to neurodegeneration. Our recent study found that lipoxin B4 (LXB4), produced by retinal astrocytes, has direct neuroprotective actions on retinal ganglion cells. In this study, we aimed to investigate how the autacoid LXB4 influences astrocyte reactivity in the retina under inflammatory cytokine-induced activation and during ocular hypertension. The protective activity of LXB4 was investigated in vivo using the mouse silicone-oil model of chronic ocular hypertension. By employing a range of analytical techniques, including bulk RNA-seq, RNAscope in-situ hybridization, qPCR, and lipidomic analyses, we discovered the formation of lipoxins and expression of the lipoxin pathway in rodents (including the retina and optic nerve), primates (optic nerve), and human brain astrocytes, indicating the presence of this neuroprotective pathway across various species. Findings in the mouse retina identified significant dysregulation of the lipoxin pathway in response to chronic ocular hypertension, leading to an increase in 5-lipoxygenase (5-LOX) activity and a decrease in 15-LOX activity. This dysregulation was coincident with a marked upregulation of astrocyte reactivity. Reactive human brain astrocytes also showed a significant increase in 5-LOX. Treatment with LXB4 amplified the lipoxin biosynthetic pathway by restoring and amplifying the generation of another member of the lipoxin family, LXA4, and mitigated astrocyte reactivity in mouse retinas and human brain astrocytes. In conclusion, the lipoxin pathway is functionally expressed in rodents, primates, and human astrocytes, and is a resident neuroprotective pathway that is downregulated in reactive astrocytes. Novel cellular targets for LXB4's neuroprotective action are inhibition of astrocyte reactivity and restoration of lipoxin generation. Amplifying the lipoxin pathway is a potential target to disrupt or prevent astrocyte reactivity in neurodegenerative diseases, including retinal ganglion cell death in glaucoma.

Normal diameter of the optic nerve using magnetic resonance imaging: A retrospective Nigerian study.

PURPOSE: The variations in the diameter of the optic nerve (ON) are important clinically in the diagnosis of conditions associated with the ON such as raised intracranial pressure, meningioma, optic neuritis, and Grave's orbitopathy. This study determined the normal diameters of the ON in adult Nigerians seen in a Hospital in Delta State. METHODS: Axial T1-weighted brain magnetic resonance imaging images of 150 patients (75 males and 75 females) aged ≥20 years were retrieved from the hospital's radiological database and retrospectively used to evaluate the diameter of the ON on axial and coronal sections. The data were analyzed and summarized using descriptive statistics. The mean diameters were compared based on gender, side, and age groups and correlated with age using inferential statistics. The significance level was considered at 5%. RESULTS: The diameter of the ON measured 0.45 ± 0.07 cm on the coronal section, besides 0.50 ± 0.07 cm, and 0.46 ± 0.06 cm at 0.3 cm and 0.8 cm from the posterior pole of the globe, respectively, on the axial slices. The diameters were significantly larger in males than in females (P < 0.05) and were symmetrical. However, they lacked significant association with age (P > 0.05). The three diameters measured had a significant positive correlation with each other (P < 0.05). CONCLUSION: The study provides a normal range of ON diameter in the study center to aid in the diagnosis of raised intracranial pressure and pathologies involving the nerve and its sheath.

Effect of astrocyte GPER on the optic nerve inflammatory response following optic nerve injury in mice.

Activated astrocytes are a primary source of inflammatory factors following traumatic optic neuropathy (TON). Accumulation of inflammatory factors in this context leads to increased axonal damage and loss of retinal ganglion cells (RGCs). Therefore, in the present study, we explored the role of the astrocyte G protein-coupled estrogen receptor (GPER) in regulating inflammatory factors following optic nerve crush (ONC), and analyzed its potential regulatory mechanisms. Overall, our results showed that GPER was abundantly expressed in the optic nerve, and co-localized with glial fibrillary acidic proteins (GFAP). Exogenous administration of G-1 led to a significant reduction in astrocyte activation and expression of inflammation-related factors (including IL-1ß, TNF-α, NFκB, and p-NFκB). Additionally, it dramatically increased the survival of RGCs. In contrast, astrocytes were activated to a greater extent by exogenous G15 administration; however, RGCs survival was significantly reduced. In vitro, GPER activation significantly reduced astrocyte activation and the release of inflammation-related factors. In conclusion, activation of astrocyte GPER significantly reduced ONC inflammation levels, and should be explored as a potential target pathway for protecting the optic nerve and RGCs after TON.