scholarly journals BPC 157 as a Therapy for Retinal Ischemia Induced by Retrobulbar Application of L-NAME in Rats

2021 ◽  
Vol 12 ◽  
Author(s):  
Mirna Zlatar ◽  
Antonio Kokot ◽  
Lovorka Batelja Vuletic ◽  
Sanja Masnec ◽  
Tamara Kralj ◽  
...  
Keyword(s):  
Blood Vessels ◽  
Optic Disc ◽  
Retinal Thickness ◽  
Plexiform Layer ◽  
Retinal Ischemia ◽  
Inner Plexiform Layer ◽  
Single Application ◽  
Bpc 157 ◽  
Severe Stage ◽  
Pentadecapeptide Bpc 157

Providing NO-system importance, we suggest that one single application of the NOS-blocker L-NAME may induce retinal ischemia in rats, and that the stable pentadecapeptide BPC 157 may be the therapy, since it may interact with the NO-system and may counteract various adverse effects of L-NAME application. A rat retinal ischemia study was conducted throughout 4 weeks, including fundoscopy, behavior presentation, tonometry, and histology assessment. Retrobulbar L-NAME application (5 mg/kg; 0.5 mg/0.1 ml saline/each eye) in rats immediately produced moderate generalized irregularity in the diameter of blood vessels with moderate atrophy of the optic disc and faint presentation of the choroidal blood vessels, and these lesions rapidly progressed to the severe stage. The specific L-NAME–induced vascular failure points to normal intraocular pressure (except to very transitory increase upon drug retrobulbar administration). When BPC 157 (10 μg; 10 ng/kg, as retrobulbar application, 1 μg; 1 ng/0.1 ml saline/each eye) is given at either 20 min after L-NAME or, lately, at 48 h after L-NAME, the regular retrobulbar L-NAME injection findings disappear. Instead, fundoscopy demonstrated only discrete generalized vessel caliber irregularity with mild atrophy of the optic disc, and then, quite rapidly, normal eye background and choroidal blood vessels, which remain in all of the subsequent periods. Also, histology assessment at 1, 2, and 4 weeks shows that BPC 157 counteracted the damaged inner plexiform layer and inner nuclear layer, and revealed normal retinal thickness. The poor behavioral presentation was also rescued. Thus, while further studies will be done, BPC 157 counteracted L-NAME–induced rat retinal ischemia.

scholarly journals Custom extraction of macular ganglion cell-inner plexiform layer thickness more precisely co-localizes structural measurements with visual fields test grids

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Janelle Tong ◽  
David Alonso-Caneiro ◽  
Nayuta Yoshioka ◽  
Michael Kalloniatis ◽  
Barbara Zangerl
Keyword(s):  
Ganglion Cell ◽  
Optic Disc ◽  
Visual Fields ◽  
Plexiform Layer ◽  
Inner Plexiform Layer ◽  
Spatial Direction ◽  
Healthy Cohort ◽  
Foveal Center ◽  
And Function ◽  
Thickness Measurements

Abstract We aimed to evaluate methods of extracting optical coherence tomography (OCT)-derived macular ganglion cell-inner plexiform layer (GCIPL) thickness measurements over retinal locations corresponding to standard visual field (VF) test grids. A custom algorithm was developed to automatically extract GCIPL thickness measurements from locations corresponding to Humphrey Field Analyser 10-2 and 30-2 test grids over Goldmann II, III and V stimulus sizes from a healthy cohort of 478 participants. Differences between GCIPL thickness measurements based on VF test grids (VF-based paradigms) and the 8 × 8 grid, as per instrument review software, were analyzed, as were impacts of fovea to optic disc tilt and areas over which GCIPL thickness measurements were extracted. Significant differences between the VF-based paradigms and the 8 × 8 grid were observed at up to 55% of locations across the macula, with the greatest deviations at the fovea (median 25.5 μm, 95% CI 25.24–25.72 μm, P < .0001). While significant correlations with fovea to optic disc tilt were noted at up to 33% of locations distributed 6°–8° from the foveal center, there were no marked differences in GCIPL thickness measurements between VF-based paradigms using different stimulus sizes. As such, standard high-density OCT measurement paradigms do not adequately reflect GCIPL measurements at retinal locations tested with standard VF patterns, with the central macular region contributing most to the observed differences and with further correction required for fovea to optic disc tilt. Spatial direction of GCIPL thickness measurements will improve future comparisons of structure and function, thereby improving methods designed to detect pathology affecting the inner retina.

scholarly journals Correlation between Macular Pigment Optical Density and Neural Thickness and Volume of the Retina

Nutrients ◽  
2020 ◽  
Vol 12 (4) ◽  
pp. 888
Author(s):  
Norihiro Nagai ◽  
Teru Asato ◽  
Sakiko Minami ◽  
Misa Suzuki ◽  
Hajime Shinoda ◽  
...  
Keyword(s):  
Optical Density ◽  
Retinal Thickness ◽  
Outer Nuclear Layer ◽  
Plexiform Layer ◽  
Macular Pigment ◽  
Inner Plexiform Layer ◽  
The Mean ◽  
Short Wavelength Light ◽  
The Impact ◽  
Adult Volunteers

Macular pigment (MP), which is composed of lutein/zeaxanthin/mezo-zeaxanthin, is concentrated in the central part of the retina, the macula. It protects the macula by absorbing short-wavelength light and suppressing oxidative stress. To evaluate whether MP levels are related to retinal neural protection and resulting health, we analyzed the association between the MP optical density (MPOD), and the macular thickness and volumes. Forty-three eyes of 43 healthy adult volunteers (21 men and 22 women; age: 22–48 (average 31.4 ± 1.1) years) were analyzed. Highly myopic eyes (<-6 diopters) were excluded. MPOD was measured using MPS2®, and the neural retinal thickness and volume were measured using optical coherence tomography. The mean MPOD was 0.589 ± 0.024, and it positively correlated with the central retinal thickness (P = 0.017, R = 0.360) and retinal volume of the fovea (1-mm diameter around the fovea; P = 0.029, R = 0.332), parafovea (1–3-mm diameter; P = 0.002, R = 0.458), and macula (6-mm diameter; P = 0.003, R = 0.447). In the macular area (diameter: 6 mm), MPOD was correlated with the retinal neural volume of the ganglion cell layer (P = 0.037, R = 0.320), inner plexiform layer (P = 0.029, R = 0.333), and outer nuclear layer (P = 0.020, R = 0.353). Thus, MPOD may help in estimating neural health. Further studies should determine the impact of MP levels on neuroprotection.

scholarly journals Transneuronal Degeneration in the Visual Pathway of Rats following Acute Retinal Ischemia/Reperfusion

2021 ◽  
Vol 2021 ◽  
pp. 1-15
Author(s):  
Yanyan Fu ◽  
Tu Hu ◽  
Qianyue Zhang ◽  
Shuhan Meng ◽  
Ying Lu ◽  
...  
Keyword(s):  
Visual Function ◽  
Ischemia Reperfusion ◽  
Plexiform Layer ◽  
Signal Propagation ◽  
Retinal Ischemia ◽  
Visual Pathways ◽  
Dorsal Lateral Geniculate Nucleus ◽  
Inner Plexiform Layer ◽  
Transneuronal Degeneration ◽  
Neuronal Soma

The maintenance of visual function not only requires the normal structure and function of neurons but also depends on the effective signal propagation of synapses in visual pathways. Synapses emerge alterations of plasticity in the early stages of neuronal damage and affect signal transmission, which leads to transneuronal degeneration. In the present study, rat model of acute retinal ischemia/reperfusion (RI/R) was established to observe the morphological changes of neuronal soma and synapses in the inner plexiform layer (IPL), outer plexiform layer (OPL), and dorsal lateral geniculate nucleus (dLGN) after retinal injury. We found transneuronal degeneration in the visual pathways following RI/R concretely presented as edema and mitochondrial hyperplasia of neuronal soma in retina, demyelination, and heterotypic protein clusters of axons in LGN. Meanwhile, small immature synapses formed, and there are asynchronous changes between pre- and postsynaptic components in synapses. This evidence demonstrated that transneuronal degeneration exists in RI/R injury, which may be one of the key reasons for the progressive deterioration of visual function after the injury is removed.

Immunohistochemical localization of GABAA receptors in the retina of the new world primate Saimiri sciureus

1989 ◽  
Vol 2 (6) ◽  
pp. 565-581 ◽  
Author(s):  
Thomas E. Hughes ◽  
Russell G. Carey ◽  
Javier Vitorica ◽  
Angel L. de Blas ◽  
Harvey J. Karten
Keyword(s):  
Monoclonal Antibody ◽  
Optic Disc ◽  
New World ◽  
Ganglion Cells ◽  
Large Population ◽  
Plexiform Layer ◽  
Amacrine Cells ◽  
Saimiri Sciureus ◽  
Inner Plexiform Layer ◽  
World Primate

AbstractA large population of amacrine cells in the retina are thought to use GABA as an inhibitory neurotransmitter in their synaptic interactions within the inner plexiform layer. However, little is known about their synaptic targets; the neurons that express the receptors for GABA have not been clearly identified. Recently, the GABAA receptor has been isolated and antibodies have been raised against it. These antibodies have proven useful for the immunocytochemical localization of the receptor, and two brief reports describing the distribution of GABAA receptor immunoreactivity in the retina have appeared (Richards et al., 1987; Mariani et al., 1987). We used a monoclonal antibody (62–3G1) against the GABAA receptor to study the retina of the New World primate Saimiri sciureus.Labeled somata were found in the inner nuclear layer (INL) and ganglion cell layer (GCL). The staining was confined to what appeared to be the cell's plasmalemma and small cytoplasmic granules. Most of the labeled neurons in the INL had small somata (5–7 μm in diameter) located at the vitreal edge of the layer. They arborized in two laminae (approximately 2 and 4) of inner plexiform layer (IPL). Ventral to the optic disc (2.5 mm) they comprised 29% of the cells present. A few of the labeled neurons appeared to be interplexiform cells or flat bipolar cells, with labeled processes that extended into both the IPL and the inner half of the outer plexiform layer. In the GCL, the labeled somata were among the largest present (13–20 μm in diameter), and 2.5 mm ventral to the optic disc they made up 15% of the cells present. Experiments in which immunoreactive somata were retrogradely labeled following the injection of fluorescent tracers into the optic tract provided a conclusive demonstration that some of the immunoreactive somata were ganglion cells. The antibody often labeled their axons in the optic fiber layer. This suggests that the GABAA receptors are transported anterogradely to the retinal terminal fields. The dendrites of the immunoreactive ganglion cells extended into the 2 laminae of labeled processes in the IPL, and their primary dendritic arbors were, at any given eccentricity, quite similar in appearance. This homogeneity suggests that they comprise a particular subset of the ganglion cells.Sections simultaneously labeled with the monoclonal antibody against the GABAA receptor and antisera against either L-glutamic acid decarboxylase (GAD) or GABA revealed that the GAD/GABA was distributed much more widely in the IPL than the GABAA receptor. This variance may reflect either the presence of other, perhaps GABAB, receptors in the IPL or GABA in portions of the IPL where it is ineffective as a neurotransmitter.

Relationship between ganglion cell-inner plexiform layer and optic disc/retinal nerve fibre layer parameters in non-glaucomatous eyes

2013 ◽  
Vol 97 (12) ◽  
pp. 1592-1597 ◽  
Author(s):  
Yih-Chung Tham ◽  
Carol Y Cheung ◽  
Victor T Koh ◽  
Ching-Yu Cheng ◽  
Elizabeth Sidhartha ◽  
...  
Keyword(s):  
Ganglion Cell ◽  
Optic Disc ◽  
Nerve Fibre ◽  
Plexiform Layer ◽  
Retinal Nerve Fibre Layer ◽  
Inner Plexiform Layer ◽  
Fibre Layer ◽  
Nerve Fibre Layer

scholarly journals Impact of tafluprost and tafluprost/timolol on the thickness of the retina in the macular area

2019 ◽  
Vol 12 (1) ◽  
pp. 18-24
Author(s):  
N. I. Kurysheva ◽  
E. V. Polunina ◽  
D. D. Arzhukhanov ◽  
A. M. Tkhamadokova
Keyword(s):  
Macular Edema ◽  
Retinal Thickness ◽  
Open Angle Glaucoma ◽  
Pigment Epithelium ◽  
Plexiform Layer ◽  
Treated Group ◽  
Reference Level ◽  
Control Group ◽  
Inner Plexiform Layer ◽  
Macular Area

Prostaglandinanalogues (PAs) are the drugs of choice in the treatment of primary open-angle glaucoma (POAG). However, they have pro-inflammatory properties and may cause macular edema. Tafluprost is the first PA to be free of preservatives. The efficacy and safety of tafluprost, as well as that of tafluprost/timolol fixed combination (FC), was demonstrated in randomized multicenter trials. However, there are no literary data concerning the effect of tafluprost and its FC on the thickness of the macula.Purpose. To assess the effect of tafluprost and tafloprost/timolol on the retinal thickness in the macular area in patients with POAG.Material and methods. The retinal thickness (RT) was measured with an interval of a week in 36 patients (36 eyes) with a newly diagnosed initial stage of POAG, 12 of whom were prescribed taflotan, 12 patients received tafluprost/timolol FC, and 12 eyes represented the control group (no drugs were prescribed). The measurements were performed in the macular area using a spectral domain optical coherence tomography (SD-OCT) by means of the RtVue xR Avanti with the AngioVue OCT angiography function. The change in the intraocular pressure (IOP) and RT from the inner limiting membrane (ILM) to the inner plexiform layer (inner retina) and to the pigment epithelium (PE) in fovea and parafovea in total and by sectors were estimated by comparing paired repeated observations using the median growth analysis.Results. In the tafluprost group, a 19.4 % IOP decrease was revealed and in the tafluprost/timolol group the decrease achieved 43 % with respect to the reference level. In patients receiving tafluprost, an increase in the RT in parafovea was noted: median growth 2 μm (p = 0.035); and in patients receiving tafluprost/timolol — in the inner layers of parafovea: median growth 3 μm (p = 0.031), and its inferior half: median growth 2.5 μm (p = 0.023). These changes were obtained in 10 patients out of 12 in each treated group. In untreated patients, the RT remained unchanged. The visual acuity did not change in any group of patients.Conclusions. In patients with glaucoma, a thickening of both the inner layers and the entire macular retina occurred within a week after treating with tafluprost or its FC, leaving no clinical manifestation. This fact should be taken into account in patients likely to develop macular edema.

The Protective Effects of Melatonin, Vitamin E and Octreotide on Retinal Edema during Ischemia-Reperfusion in the Guinea Pig Retina

2002 ◽  
Vol 12 (6) ◽  
pp. 443-449 ◽  
Author(s):  
T. Yilmaz ◽  
S. Çelebi ◽  
A.Ş. Kükner
Keyword(s):  
Vitamin E ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Plexiform Layer ◽  
Retinal Ischemia ◽  
Control Group ◽  
Inner Plexiform Layer ◽  
Free Radical Damage ◽  
Microscopic Evaluation ◽  
Group 1

Purpose The purpose of this study is to provide evidence that free radical damage is a component of retinal ischemia-reperfusion (I/R) injury, and to determine whether melatonin, vitamin E and octreotide can protect retina from this injury. Methods The right eyes of 50 male guinea pigs weighing 500–600 g were used. The animals were randomly assigned to group 1 (control), group 2 (I/R), group 3 (melatonin + I/R), group 4 (vitamin E + I/R) and group 5 (octreotide + I/R). Groups 3, 4 and 5 received four subcutaneous injections at six-hour intervals for total dosage of 10 mg/kg melatonin, 150 mg/kg vitamin E and 22 μg/kg octreotide respectively. The first dose of each substance was administered 5 minutes before retinal ischemia. Retinal ischemia was induced for 1.5 hours, then followed by reperfusion for 24 hours. Infections of all three substances were repeated at 6, 12 and 18 hours during reperfusion. The animals were killed at 24 hours of reperfusion. Sagittal sections of 4 μm were cut and stained with hematoxylin and eosin for light microscopic evaluation. The average thickness (edema) of the inner plexiform layer for each eye was measured in sagittal sections near the optic nerve and expressed in microns. Results The efficacy of each compound had the following relationships: melatonin>vitamin E>octreotide in preventing retinal damage by ischemia-reperfusion. The mean thickness of the inner plexiform layer was 13.3 ± 0.8 μm, 25.9 ± 2.0 μm, 20.0 ± 0.7 μm, 21.6 ± 0.7 μm, 23.9 ± 0.8 μm respectively in the control, I/R, I/R plus melatonin, I/R plus vitamin E and I/R plus octreotide groups. The thickness of the inner plexiform layer in group 1 (control) was significantly less than the other groups (p<0.001). The inner plexiform layer was thicker in the I/R group than with I/R plus melatonin, I/R plus vitamin E and I/R plus octreotide (all p <0.01). The inner plexiform layer was thicker in the I/R plus octreotide group than the I/R plus vitamin E and I/R plus melatonin groups both (p<0.05). Compared to the I/R plus melatonin group, the inner plexiform layer was significantly thicker in the I/R plus vitamin E group (p<0.05). Conclusions This study demonstrates a protective effect of melatonin, vitamin E and octreotide on the retina during retinal ischemia-reperfusion injury.

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