Optic Ganglion Research Articles

Functional eye rudiments in the anchialine crab Munidopsis polymorpha (Crustacea: Galatheidae)

Abstract The white crab Munidopsis polymorpha (Crustacea: Galatheidae) is the only one of a species-rich genus not occurring in the deep sea. It is endemic to marine caves, anchialine pools and groundwaters of the volcanic island of Lanzarote (Canary Islands). The eye derives from the superposition type possessing a clear zone formed by the proximal extensions of the rudimentary crystalline cones. The number of ommatidia ranges among the lowest found in decapods and the optic ganglia are strongly diminished in size. The crystalline cones are rudimentary or lost and facets with individual corneas are not discernible. The rhabdoms are tiny and irregularly arranged in the rhabdom layer. Some rhabdoms display an open arrangement of rhabdomers with microvilli that are not aligned to form orthogonal layers. The eye is one of the rare exceptions of traits that despite being rudimentary is still partially functional. The absence of stabilizing selection is probably the reason for variability or reduction of the traits necessary for image formation. In contrast, negative phototactic behaviour is present, because light is still perceived by the eyes of M. polymorpha.

Comprehensive visual electrophysiological measurements discover crucial changes caused by alcohol addiction in humans: Clinical values in early prevention of alcoholic vision decline.

Alcohol addiction often compromises vision by impairing the visual pathway, particularly the retina and optic nerve. Vision decline in alcoholics consists of a sequential transition from reversible functional deterioration of the visual pathway to irreversible clinical vision degeneration or vision loss. Thus, the control of alcoholic vision decline should focus on prevention before permanent damage occurs. Visual electrophysiology is a promising method for early detection of retinal dysfunction and optic neuropathy, including full-field electroretinography (ffERG) and pattern-reversal visual evoked potential (PR-VEP). So far, however, research studying the electrophysiological characteristics in the preclinical stage of vision decline caused by alcohol addiction is still lacking. Here we conducted a retrospective study with 11 alcoholics and 14 matched control individuals to address this need. We had performed comprehensive visual electrophysiological tests, including ffERG and PR-VEP. We next analyzed all electrophysiological parameters using multivariate statistical analyses and discovered some highly sensitive alterations to alcohol addiction. We found severely reduced amplitudes in scotopic ffERG oscillatory potentials (OPs) in alcohol addicts. These changes indicate the alcohol-induced disturbances of amacrine cells and retinal circulation. In subjects with alcohol addiction, the amplitudes of b-waves diminish significantly in scotopic but not photopic ffERG, implying the impaired function of the retinal rod system and the dysfunction of the inner retina. PR-VEPs elicited by checkerboard stimuli with large 1 degree (°) checks mainly reflect the state of the optic nerve and ganglion cells, and PR-VEPs provoked by small 0.25° checks mainly reflect the function of the macular. We performed both measurements and observed a robust amplitude reduction in all three peaks (N75–P100, P100–N135) and a significant peak time extension in P100. Our research provides an affordable and non-invasive tool to accurately evaluate visual pathway conditions in alcohol addicts and help clinicians take targeted treatment.

Improved Ophthalmic Outcomes Following Venous Sinus Stenting in Idiopathic Intracranial Hypertension.

Ophthalmic outcomes following venous sinus stenting (VSS) in patients with idiopathic intracranial hypertension (IIH) are not well characterized. A retrospective chart review was conducted on 86 consecutive patients with IIH who underwent venous sinus stenting at Mayo Clinic, Rochester, Minnesota and Stanford Medical Center, Palo Alto, California between May 2015 and October 2021. Patients with raised intracranial pressure from a non-IIH etiology were excluded. Clinical symptoms and neuro-ophthalmological data, including best corrected visual acuity (BCVA), visual field mean deviation, papilledema, and optical coherence tomography (OCT) peripapillary retinal nerve fiber layer (pRNFL) and ganglion cell inner plexiform layer (GC-IPL), were analyzed. Baseline measurements before VSS and 3 months or more postoperatively were compared. Eighty-six subjects (82 female) were included in this study, with a median age of 33 (16-68) years and a median body mass index of 36.69 (22.30-62.00) kg/m2. 85/86 (98.8%) had attempted prior management with medication, and 12/86 (14%) had prior surgical management with optic nerve sheath fenestration, ventriculoperitoneal shunt, or bariatric surgery. Prior to VSS, 67/86 (77.9%) had papilledema, 85/86 (98.8%) had headaches, and 68/86 (79.1%) had pulsatile tinnitus. For patients with both pre- and post-VSS data available, the average papilledema grade was 1.76 (0-5) (n = 74) and the average OCT pRNFL was 186.34 (52.00-588.00) µm (n = 70), prior to VSS. A median of 4.0 (interquartile range 3.3-5.4) months after VSS, the average papilledema grade improved to 0.39 (0-2), p <0.001, and OCT pRNFL improved to 96.86 (47.00-168.00) µm, p <0.001. 28/86 (32.6%) patients no longer required medication for high intracranial pressure. 14/85 (16.5%) patients reported complete resolution of their headache and 55/71 (77.5%) reported improvement in headache quality. 40/68 (66.7%) reported complete resolution of pulsatile tinnitus. OCT GC-IPL, BCVA, and visual field mean deviation did not significantly change pre- vs post-VSS. Our large consecutive case series corroborates smaller prior studies in demonstrating the overall efficacy of VSS for patients with IIH. We found both ophthalmic improvements, as demonstrated by the significantly reduced papilledema and pRNFL, and overall clinical symptom improvement.

Connectome of the lamina reveals the circuit for early color processing in the visual pathway of a butterfly

Connectomics has become a standard neuroscience methodology in a few model animals,1 with the visual system being a popular target of study.2-5 Combining connectomics with circuit and behavioral physiology, recent studies on the color vision of the fruit fly Drosophila melanogaster have focused on the mechanisms underlying early wavelength processing in the optic ganglia.6-8 However, the color vision capabilities of D.melanogaster are limited,9 compared with many flower-visiting insects.10,11 For example, a butterfly Papilio xuthus has six spectral classes of photoreceptors. Each ommatidium contains nine photoreceptors in one of three fixed combinations, making the eye an array of three spectrally distinct ommatidia types.12 Behaviorally, P.xuthus can detect 1nm differences in light wavelength across the spectrum from ultraviolet to red, outperforming humans.13 What is the neuronal basis of such precise color vision? How does such a system evolve? Addressing these questions requires comparative studies at the circuit level. Here, we performed a connectome analysis in the first optic ganglion, the lamina, of P.xuthus. The lamina comprises cartridges, each typically containing nine photoreceptor axons from a single ommatidium and four second-order neurons. We found abundant inter-photoreceptor connections, which are absent in the lamina of D.melanogaster. We also identified connections between neighboring cartridges, particularly those receiving inputs from spectrally distinct ommatidia. The linear summation of synaptic connections well explains the spectral sensitivity of photoreceptors and second-order neurons in the lamina.

Diagnostic utility of the optical coherence tomography ganglion cell complex in diagnosing Leber's hereditary optic neuropathy masquerading as functional vision loss

Diagnostic utility of the optical coherence tomography ganglion cell complex in diagnosing Leber's hereditary optic neuropathy masquerading as functional vision loss

Measurement of electroretinogram responses in OPA1‐associated autosomal dominant optic atrophy using a handheld device

AbstractPurposeAutosomal dominant optic atrophy (ADOA) associated with OPA1 variants is the most common inherited optic neuropathy in the population. The utility of the Ganzfeld electroretinogram (ERG) in evaluating ADOA has not been extensively investigated. In this study, we explored the potential of using a handheld ERG device (RETeval®) to measure ERG responses in a cohort of patients with ADOA carrying pathogenic OPA1 mutations.MethodsThe Ganzfeld photopic ERG was recorded in 15 individuals with OPA1‐associated ADOA in response to series of flashes (200, automatically adjusted in intensity to pupil diameter) using the RETeval® handheld ERG device and skin electrodes. Two to three series were obtained from each eye. The recordings were analysed for noise and drift manually. Both visual acuity measurements, and optical coherence tomography ganglion cell layer (GCL) and retina nerve fibre layer (RNFL) thicknesses were recorded to explore correlation with ERG parameters.ResultsThere was a significant correlation between LogMAR visual acuity and both the a‐wave (ρ = ‐0.60, p = 0.02, n = 15) and b‐wave (ρ = ‐0.54, p = 0.04, n = 15) peak times. As a‐wave and b‐wave peak time correlated with age, a multiple linear regression analysis was performed to exclude age as a confounder. With respect to the a‐wave analysis, the coefficients for visual acuity and age were ‐0.66 (p = 0.019) and 0.015 (p = 0.14), respectively. With respect to b‐wave analysis, the coefficients for visual acuity and age were ‐1.32 (p = 0.017) and 0.028 (p = 0.16), respectively. There was no significant correlation between a‐wave and b‐wave peak times with the OCT structural parameters that were analysed.ConclusionsIn patients with OPA1‐associated ADOA, a‐wave and b‐wave peak times correlated negatively with LogMAR visual acuity, independent of the effects of age. The pathophysiological relevance of these findings requires further investigation in a larger patient cohort.

Incidence of Primary Open-Angle Glaucoma at the Flamboyants Communal Medical Center of Conakry, Guinea

Background: Primary Open-Angle Glaucoma (POAG) is a chronic, progressive optic neuropathy of multifactorial origin defined by alterations in the visual field, progressive loss of optic nerve fibers and ganglion cells, and an open iridocorneal angle in gonioscopy. It is the world’s leading cause of irreversible blindness. There is no epidemiological study in Guinea that allows us to locate the real level of the problem. The objective of this study is to determine the hospital incidence of POAG at the Centre Médical Communal (CMC) in the Flamboyants. Patients and Method: This was a descriptive cross-sectional study with a prospective collection for one year, from April 1, 2020 to March 31, 2021, in patients aged at least 40 years, received in consultation at the CMC in the Flamboyants. The diagnostic criterion for a new case of glaucoma was the presence in a patient of the following two signs: (excavation of the optical disc C/D ≥ 0.5 and alteration of the visual field) with an open angle at least stage 4 of the Shaffer and Etienne classification associated or not with ocular hypertonia and having never received anti glaucoma treatment. We described variables related to sociodemographic characteristics, visual acuity, intraocular pressures, papillary excavations, and visual field surveys. Informed consent from patients was sought and obtained. The confidentiality of the files was guaranteed. Results: 68 new cases of POAG were diagnosed out of 3220 consultations, an incidence rate of 2.11%. The average age was 58.2 years (10.64 with a male predominance of 63.23%. A family history of glaucoma was present in 11.36% of cases. Visual acuity was poor < 1/10 in 79 eyes/136, average between 1/10 and 3/10 in 11 eyes/136, and good ≥ 3/10 in 46 eyes/136. The mean intraocular pressure (IOP) was 26.5 mm Hg in the right eye and 25.9 mm Hg in the left eye with extremes of 18 and 38 mm Hg. The cup/disk ratio was above 0.5 in 97.1% at OD and 95.58% at OG. The visual field was impaired in all patients. Conclusion: This study has shown us that POAG in our environment is relatively common, early onset, and rapidly evolving. The implementation of a rapid and reliable screening strategy by the Eye Health Program will make it possible to manage glaucoma from the earliest stages.

CD82 protects against glaucomatous axonal transport deficits via mTORC1 activation in mice

Glaucoma is a leading cause of irreversible blindness worldwide and is characterized by progressive optic nerve degeneration and retinal ganglion cell loss. Axonal transport deficits have been demonstrated to be the earliest crucial pathophysiological changes underlying axonal degeneration in glaucoma. Here, we explored the role of the tetraspanin superfamily member CD82 in an acute ocular hypertension model. We found a transient downregulation of CD82 after acute IOP elevation, with parallel emergence of axonal transport deficits. The overexpression of CD82 with an AAV2/9 vector in the mouse retina improved optic nerve axonal transport and ameliorated subsequent axon degeneration. Moreover, the CD82 overexpression stimulated optic nerve regeneration and restored vision in a mouse optic nerve crush model. CD82 exerted a protective effect through the upregulation of TRAF2, which is an E3 ubiquitin ligase, and activated mTORC1 through K63-linked ubiquitylation and intracellular repositioning of Raptor. Therefore, our study offers deeper insight into the tetraspanin superfamily and demonstrates a potential neuroprotective strategy in glaucoma treatment.

The Lack of Amyloidogenic Activity Is Persistent in Old WT and APPswe/PS1ΔE9 Mouse Retinae.

We have previously reported that vision decline was not associated with amyloidogenesis processing in aging C57BL/6J wild-type (WT) mice and in a mouse model of Alzheimer’s disease, the APPswe/PS1ΔE9 transgenic mouse model (APP/PS1). This conclusion was drawn using middle-aged (10–13 months old) mice. Here, we hypothesized that compared with hippocampal and cortical neurons, the weak amyloidogenic activity of retinal neurons may result in a detectable release of amyloid β (Aβ) only in aged mice, i.e., between 14 and 24 months of age. The aim of the present study was thus to follow potential activity changes in the amyloidogenic and nonamyloidogenic pathways of young (4 months) and old (20–24 months) WT and APP/PS1 mice. Our results showed that in spite of retinal activity loss reported by electroretinogram (ERG) recordings, the level of amyloid beta precursor protein (APP) and its derivatives did not significantly vary in the eyes of old vs. young mice. Strikingly, the ectopic expression of human APPswe in APP/PS1 mice did not allow us to detect Aβ monomers at 23 months. In contrast, Aβ was observed in hippocampal and cortical tissues at this age but not at 4 months of life. In contrast, optic nerve transection-induced retinal ganglion cell injury significantly affected the level of retinal APP and the secretion of soluble APP alpha in the vitreous. Collectively, these results suggest that the amyloidogenic and nonamyloidogenic pathways are not involved in visual function decline in aging mice. In WT and APP/PS1 mice, it is proposed that retinal neurons do not have the capacity to secrete Aβ in contrast with other cortical and hippocampal neurons.

Management of toxic optic neuropathy via a combination of Wharton\u2019s jelly-derived mesenchymal stem cells with electromagnetic stimulation

PurposeTo investigate the effect of the combination of Wharton's jelly derived mesenchymal stem cells (WJ-MSC) and high frequency repetitive electromagnetic stimulation (rEMS) in the therapy of toxic optic neuropathies with severe symptoms after the available current therapy modalities which were unsucessful.Material and methodsThis prospective, open-label clinical phase-3 study was conducted at Ankara University Faculty of Medicine, Department of Ophthalmology between April 2019 and April 2021. Thirty-six eyes of 18 patients with toxic optic neuropathy (TON) were included in the study. Within 1–3 months after the emergency interventions, patients with various degrees of sequela visual disturbances were studied in this clinical trial. The cases were divided into three groups according to similar demographic characteristics. Group 1: Consists of 12 eyes of 12 patients treated with the WJ-MSC and rEMS combination in one eye. Group 2: Consists of 12 eyes of 12 patients treated with only rEMS in one eye. Group 3: Consists of 12 eyes of six patients treated with only WJ-MSC in both eyes. The course was evaluated by comparing the quantitive functional and structural assessment parameters measured before and at the fourth month of applications in each group.ResultsThe mean best corrected visual acuity (BCVA) delta change percentages of the groups can be ranked as: Group 1 (47%) > Group 3 (32%) > Group 2 (21%). The mean fundus perimetry deviation index (FPDI) delta change percentages of the groups can be ranked as: Group 1 (95%) > Group 2 (33%) > Group 3 (27%). The mean ganglion cell complex (GCC) thickness delta change (decrease in thickness) percentages can be ranked as: Group 1 (− 21%) > Group 3 (− 15%) > Group 2 (− 13%). The visual evoked potential (VEP) P100 latency delta change percentages of the groups can be ranked as: Group 1 (− 18%) > Group 3 (− 10%) > Group 2 (− 8%). The P100 amplitude delta change percentages of the groups can be ranked as: Group 1 (105%) > Group 3 (83%) > Group 2 (24%).ConclusionToxic optic neuropathies are emergent pathologies that can result in acute and permanent blindness. After poisoning with toxic substances, progressive apoptosis continues in optic nerve axons and ganglion cells. After the proper first systemic intervention in intensive care clinic, the WJ-MSC and rEMS combination seems very effective in the short-term period in cases with TON. To prevent permanent blindness, a combination of WJ-MSC and rEMS application as soon as possible may increase the chance of success in currently untreatable cases.Trial Registration ClinicalTrials.gov ID: NCT04877067.

Optical Microangiography and Progressive Retinal Nerve Fiber Layer Loss in Primary Open Angle Glaucoma

To evaluate the association between optical microangiography (OMAG) measurements and progressive retinal nerve fiber layer (RNFL) loss in primary open angle glaucoma (POAG). Prospective case series. Sixty-four eyes of 40 patients with POAG (108 quadrants) with mild to moderate functional damage were longitudinally studied for at least 2 years and with a minimum of 3 optical coherence tomography examinations. OMAG imaging was performed at the baseline visit. Effect of clinical parameters (age, sex, presence of systemic diseases, central corneal thickness, presence of disc hemorrhage, and mean and fluctuation of intraocular pressure during follow-up), baseline hemifield mean deviation, baseline quadrant optical coherence tomography RNFL and ganglion cell inner plexiform layer thickness), and OMAG (peripapillary and macular perfusion density [PD] and vessel density [VD]) on the rate of RNFL change was evaluated using linear mixed models. Average (±SD) mean deviation, RNFL, and ganglion cell inner plexiform layer thickness of the analyzed quadrants at baseline were -5.5 ± 2.9 dB, 96.5 ± 17.9 µm, and 73.8 ± 8.6 µm, respectively. Peripapillary PD and VD in the quadrant were 44.6% ± 5.9% and 17.5 ± 2.2 mm/mm2, respectively. Rate of quadrant RNFL change was -1.8 ± 0.6 µm/y. Multivariate mixed models showed that lower peripapillary PD (coefficient=0.08, P=.01) and lower VD (coefficient=0.21, P=.02) were significantly associated with a faster rate of RNFL loss. Lower baseline peripapillary PD and VD measured using OMAG were significantly associated with a faster rate of RNFL loss in POAG. OMAG imaging provides useful information about the risk of glaucoma progression and the rate of disease worsening.

Rapid homonymous hemi-macular atrophy of the optical coherence tomography ganglion cell complex after stroke

A 44-year-old man developed sudden-onset right-sided weakness, aphasia and blurred vision after a cardiac valvuloplasty. Initial CT and CT angiography of the head showed early ischaemic changes involving the left...

Characterization of prostanoid pathway and the control of its activity by the eyestalk optic ganglion in the female giant freshwater prawn, Macrobrachium rosenbergii

The giant freshwater prawn, Macrobrachium rosenbergii, is an economically valuable species that are distributed throughout the Asia-Pacific region. With the natural population declining due to overfishing, aquaculture of this species is deemed necessary. Hence, it is essential to understand the mechanisms regulating reproduction in order to increase their production. Prostaglandins (PGs) play an important role in reproduction in most vertebrates and several invertebrates. It has been proposed that crustaceans have PGs but the prostanoids pathway in the giant freshwater prawn is still unclear. In this study, we identified 25 prostanoid-related genes involved in the biosynthesis of active prostanoids in M. rosenbergii using in silico searches of transcriptome data. Comparative analysis of encoded proteins for the MroPGES2 gene with other species was performed to confirm their evolutionary conservation. Gene expression analysis revealed the correlation of MroPGES2 gene expression level with the progress of ovarian development. Eyestalk ablation increased the expression level of MroPGES2 gene compared to intact groups during the ovary maturation stages. Collectively, this study confirmed the existence of prostanoids in the giant freshwater prawn, as well as characterizing key gene MroPGES2 associated with the prostanoid pathway. We propose that MroPGES2 may play an important role in M. rosenbergii ovarian maturation and its expression is under the inhibitory control from the eyestalk optic ganglion hormones. Identification of genes in prostanoid pathway and their expressions enables future functional studies to be performed, which may lead to applications in the aquaculture of this species.

Клинический случай впервые выявленной далекозашедшей первичной открытоугольной глаукомы на фоне друз диска зрительного нерва

Aim. To present a clinical case of glaucoma development against the background of optic disc drusen (ODD), demonstrating the difficulties of differential diagnosis between such nosologies as glaucomatous optic neuropathy, optic disc swelling, and chronic optic neuropathy caused by ODD. Methods. Patient S., 72 years old, was referred to clinic with suspected optic disc swelling, initial senile cataract of both eyes. The patient underwent additional investigations: Maklakov tonometry registered an increase of intraocular pressure level exceeding permissible norm; perimetry which has revealed narrowing of visual field boundaries in both eyes; ß-scan ultrasonography has visualized morphological changes with highly reflective drusen in both eyes; optical coherence tomography of optic nerve and ganglion cell layer revealed decrease in nerve fiber layer thickness on nasal side. For differential diagnosis, the patient underwent magnetic resonance imaging (MRI) of the brain, according to which intracranial pathology was excluded. Results. Using modern diagnostic methods it was possible to establish clinical diagnosis: newly detected primary open-angle glaucoma (POAG) III b, explicit ODD, initial senile cataract, pseudoexfoliation syndrome grade 2. Hypotensive regimen did not result in target pressure; therefore, the patient was prescribed surgical treatment (microinvasive non-penetrating deep sclerectomy on both eyes). Conclusion. The presented clinical case showed that against the background of ODD creating the picture of pseudo-swelling and masking the changes in optic nerve because of glaucoma process, the patient had POAG in far-advanced stage. MRI of the brain, as well as additional ophthalmological investigations using modern technologies, made it possible to establish correct diagnosis and prescribe the necessary therapy for this nosology. Key words: optic disc drusen; primary open-angle glaucoma; perimetry; optical coherence tomography.

Serotonergic modulation of visual neurons in Drosophila melanogaster.

Sensory systems rely on neuromodulators, such as serotonin, to provide flexibility for information processing as stimuli vary, such as light intensity throughout the day. Serotonergic neurons broadly innervate the optic ganglia of Drosophila melanogaster, a widely used model for studying vision. It remains unclear whether serotonin modulates the physiology of interneurons in the optic ganglia. To address this question, we first mapped the expression patterns of serotonin receptors in the visual system, focusing on a subset of cells with processes in the first optic ganglion, the lamina. Serotonin receptor expression was found in several types of columnar cells in the lamina including 5-HT2B in lamina monopolar cell L2, required for spatiotemporal luminance contrast, and both 5-HT1A and 5-HT1B in T1 cells, whose function is unknown. Subcellular mapping with GFP-tagged 5-HT2B and 5-HT1A constructs indicated that these receptors localize to layer M2 of the medulla, proximal to serotonergic boutons, suggesting that the medulla neuropil is the primary site of serotonergic regulation for these neurons. Exogenous serotonin increased basal intracellular calcium in L2 terminals in layer M2 and modestly decreased the duration of visually induced calcium transients in L2 neurons following repeated dark flashes, but otherwise did not alter the calcium transients. Flies without functional 5-HT2B failed to show an increase in basal calcium in response to serotonin. 5-HT2B mutants also failed to show a change in amplitude in their response to repeated light flashes but other calcium transient parameters were relatively unaffected. While we did not detect serotonin receptor expression in L1 neurons, they, like L2, underwent serotonin-induced changes in basal calcium, presumably via interactions with other cells. These data demonstrate that serotonin modulates the physiology of interneurons involved in early visual processing in Drosophila.

Fly Feature Detectors Show Contrast Invariance, Omni-Directionality, Velocity Constancy, and Octopaminergic Loss of Background Motion Suppression

Motion vision circuits of the fly are organized into parallel ON and OFF pathways tuned to the direction and speed of motion. Directionally selective small-field columnar neurons innervate the third optic ganglion, the lobula plate, where their outputs are integrated by large dendritic fields that encode wide-field background motion. Wide-field lobula plate cells, in turn, coordinate gaze stabilization. By contrast, behavioral responses to visual features is believed to begin within the circuits of the fourth optic ganglion, the lobula. We investigated 19 lobula columnar neurons (LCs) with stimuli that are behaviorally salient to the fly. A comprehensive analysis of receptive field properties showed that LC15 encodes moving bars, whereas LC12 is relatively agnostic to object dimensions. Neither responds to optic flow, rather object responses in both LCs are suppressed by background motion. Further contrasting neurons of the motion pathway, LC12 and LC15 are both small-field cells indifferent to ON-OFF contrast polarity. LC15 responds equally to four directions of motion, whereas LC12 is selective for motion in the horizontal plane. Both are equally sensitive to object speeds ranging from 22 to 132° per second. Small objects strongly stimulate presynaptic fibers of lobula layer 2, which corresponds to the postsynaptic domains of object-detecting LCs. Finally, in direct contrast to the entire motion pathway, we were surprised to find that octopamine nullifies the inhibition of object responses generated by background motion; LC12 and LC15 remain sensitive to objects appearing against a moving background.

Long-term Kinetic Papilledema Improvement After Venous Sinus Stenting in Idiopathic Intracranial Hypertension

The aim of this study was to assess the safety and effectiveness of lateral sinus stenosis (LSS) stenting in patients with idiopathic intracranial hypertension (IIH) who are refractory to medical treatment, particularly focusing on visual outcomes including papilledema. Retrospective study of consecutive patients with IIH refractory to medical treatment who underwent LSS stenting. Clinical features, visual fields and optical coherence tomography (OCT) retinal nerve fiber layer (RNFL) and ganglion cell layer (GCL) thicknesses were assessed before stenting, at 1 month poststenting and at last follow-up. Complications were also recorded. A total of 16women were included, with amean age of 39 ± 11years. All patients had papilledema while 15/16 (94%) had headaches. Mean visual acuity was 0.036 logMAR, range (+0.4 to +0.0 logMAR). The mean RNFL thickness prior to stenting was 121.7 µm (±34.7 µm) and mean GCL thickness was 80.2 µm (±8.9 µm). Mean follow-up was 19.7months (±11.8 months). After stenting, acetazolamide was discontinued in 15/16 (94%) patients. Papilledema improved in 14/16 (88%) of patients. The mean RNFL thickness was significantly decreased 1 month after stenting (96.3 ± 15.6 µm; p < 0.001) and at last visit (93.4 ± 15.3 µm; p < 0.001). The GCL thickness after LSS stenting was moderately decreased at the last visit examination: 80.2 ± 8.9 µm vs. 78.0 ± 10.7 µm; (p < 0.01). No stent-related complication occurred, while there was one case of restenosis. Improvement of papilledema appears to occur relatively rapidly after the LSS stenting. The results further support the role of LSS stenting in the treatment of IIH, especially with respect to visual symptoms.

On the Protective Effect of Lycium Barbarum Polysaccharide (LBP) on Optic Nerve Tissue and Retinal Ganglion Cells

Background: The present paper established a model of optic neuritis injury by intrathecal injection of lipopolysaccharide (LPS) into the optic nerve, then explored the protective effect of Lycium Barbarum Polysaccharide (LBP) on optic nerve tissue and RGCs after injury. Material and methods: LPS was microinjected into the optic nerve of SD rats to induce optic neuritis. The histopathological variations of HE staining were observed in each group. The expressions of ED1/CD68 and GFAP were determined by immunofluorescence. The optic nerve repairment was evaluated by lux solid blue staining. TUNEL detects retinal cell apoptosis. Western blot was used to detect differences in expressions of related proteins. Results: LBP can alleviate the degree of optic nerve damage in rats with optic neuritis injury, inhibit the increase of LPS-induced macrophages and astrocytes in the optic nerve and retina, mitigate LPS-induced retinal RGC damage, inhibit LPS-induced expressions of proinflammatory cytokines TNF-α and IL-6, COX2 and iNOS in the optic nerve injury model of optic neuritis in rats, as well as inhibit the activation of STAT1, STAT3 and NF-κB pathways. Conclusion: LBP can ameliorate optic nerve damage, and the mechanism may be realized through inhibiting NF- B and STAT signaling pathways.

Relationship between miR-375 regulating Ndrg2/IL-6/STAT3 signaling pathway and diabetic retinopathy in rats.

To explore the relationship between micro ribonucleic acid (miR)-375 in regulating the N-Myc downstream-regulated gene 2 (Ndrg2)/interleukin-6 (IL-6)/signal transducer and activator of transcription 3 (STAT3) signaling pathway and diabetic retinopathy (DR) in rats. Thirty Sprague- Dawley rats were randomly divided into Control group (n=10), Model group (n=10), and miR-375 inhibitor group [miR-375 small interfering RNA (siRNA) group, n=10]. The rats in Model group were injected with streptozotocin (STZ) via the tail vein to prepare into rat models of diabetes. The body weight, fasting blood glucose, and retinal barrier permeability of rats in each group were detected. The levels of malondialdehyde (MDA) and superoxide dismutase (SOD) in rat serum were measured using kits. Terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate-biotin nick end labeling (TUNEL) assay was performed to determine the apoptosis of optic ganglion cells in rat retinal tissues. Additionally, the messenger RNA (mRNA) and protein levels of Ndrg2, IL-6 and STAT3 in rat retinal tissues were detected via reverse transcription-polymerase chain reaction (RT-PCR) and Western blotting, respectively. Compared with Control group, Model group had reduced body weight of rats, increased blood glucose and retinal permeability of rats, raised serum MDA content, decreased SOD activity, up-regulated apoptotic rate of optic ganglia, and notably elevated mRNA and protein levels of Ndrg2, IL-6 and STAT3 in retinal tissues. Compared with those in Model group, the body weight of rats declined, the blood glucose of rats rose, the retinal permeability of rats was decreased significantly, the serum MDA content was reduced, the SOD activity was raised, the apoptotic rate of optic ganglia was decreased, and the mRNA and protein levels of Ndrg2, IL-6 and STAT3 in retinal tissues were also decreased significantly in miR-375 siRNA group. MiR-375 inhibitors are able to reduce blood glucose, retinal permeability, and optic ganglion apoptosis in rats with DR, and the mechanism of action may be related to the regulation on the Ndrg2/IL-6/STAT3 signaling pathway.

Gene regulatory networks during the development of the Drosophila visual system.

The Drosophila visual system integrates input from 800 ommatidia and extracts different features in stereotypically connected optic ganglia. The development of the Drosophila visual system is controlled by gene regulatory networks that control the number of precursor cells, generate neuronal diversity by integrating spatial and temporal information, coordinate the timing of retinal and optic lobe cell differentiation, and determine distinct synaptic targets of each cell type. In this chapter, we describe the known gene regulatory networks involved in the development of the different parts of the visual system and explore general components in these gene networks. Finally, we discuss the advantages of the fly visual system as a model for gene regulatory network discovery in the era of single-cell transcriptomics.