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.

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.

THE NEUROPROTECTIVE EFFECTS ON RETINAL STRUCTURE BY MINOCYCLINE IN A RAT MODEL OF HIGH IOP INDUCED RETINAL ISCHEMIA INJURY

2014 ◽  
Vol 40 (02) ◽  
pp. 83-87
Author(s):  
Pei-Yun Huang ◽  
Chung-Tien Lin
Keyword(s):  
Neuroprotective Effect ◽  
Ischemia Reperfusion ◽  
Outer Nuclear Layer ◽  
Plexiform Layer ◽  
Retinal Ischemia ◽  
Control Group ◽  
Inner Plexiform Layer ◽  
Sprague Dawley ◽  
Neuroprotective Effects ◽  
Retinal Structure

The present study investigated the neuroprotective effect of minocycline, a microglial inhibitor, against the retinal ischemia–reperfusion (IR) injury in the rat. The retinal IR injury was induced in Sprague–Dawley (SD) rats by infusing normal saline into anterior chamber of eye to create a higher intraocular pressure (IOP) than blood pressure for 45 min. Minocycline (45 and 90 mg/kg/day) was administered intraperitoneally to rats receiving IR injury. The neuroprotective effects were evaluated by morphometrical histology analysis 7 days after ischemia. The data was compared with the groups treated with saline and methylprenisolone (MP, 30 mg/kg, IV). The results showed that the retinal inner plexiform layer/outer nuclear layer (IPL/ONL) ratio was reduced following IR damage compared with that in the normal control. The IPL/ONL ratio was reduced to 43.5% in the IR-control group, 93.3% and 93.6% in the Mino-45 and Mino-90 group. The IPL/ONL ratio was preserved to 95.7% in the MP group. These results suggest that minocycline and methylprednisolone showed significantly good neuroprotective effects demonstrated in retinal histology of the rats under retinal IR injury.

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 Substance P-immunoreactive neurons in hamster retinas

1999 ◽  
Vol 16 (3) ◽  
pp. 475-481 ◽  
Author(s):  
HAI-BIAO LI ◽  
KWOK-FAI SO ◽  
WAH CHEUK
Keyword(s):  
Optic Nerve ◽  
Substance P ◽  
Ganglion Cells ◽  
Plexiform Layer ◽  
Amacrine Cells ◽  
Dorsal Lateral Geniculate Nucleus ◽  
Inner Plexiform Layer ◽  
Nerve Section ◽  
Displaced Amacrine Cells ◽  
Contralateral Eye

Light-microscopic immunocytochemistry was utilized to localize the different populations of substance P-immunoreactive (SP-IR) neurons in the hamster retina. Based on observation of 2505 SP-IR neurons in transverse sections, 34% were amacrine cells whose pear-shaped or round cell bodies (7–8 μm) were situated in the inner half of the inner nuclear layer (INL) or in the inner plexiform layer (IPL), while 66% of SP-IR somata (6–20 μm) were located in the ganglion cell layer (GCL) which were interpreted to be displaced amacrine cells and retinal ganglion cells (RGCs). At least three types of SP-IR amacrine cells were identified. The SP-IR processes were distributed in strata 1, 3, and 5 with the densest plexus in stratum 5 of the inner plexiform layer. In the wholemounted retina, the SP-IR cells were found to be distributed throughout the entire retina and their mean number was estimated to be 4224 ± 76. Two experiments were performed to clarify whether any of the SP-IR neurons in the GCL were RGCs. The first experiment demonstrated the presence of SP-IR RGCs by retrogradely labeling the RGCs and subsequently staining the SP-IR cells in the retina using immunocytochemistry. The second experiment identified SP-IR central projections of RGCs to the contralateral dorsal lateral geniculate nucleus. This projection disappeared following removal of the contralateral eye. The number of SP-IR RGCs was estimated following optic nerve section. At 2 months after sectioning the optic nerve, the total number of SP-IR neurons in the GCL reduced from 4224 ± 76 to a mean of 1192 ± 139. Assuming that all SP-IR neurons in the GCL which disappeared after nerve section were RGCs, the number of SP-IR RGCs was estimated to be 3032, representing 3–4% of the total RGCs. In summary, findings of the present study provide evidence for the existence of SP-IR RGCs in the hamster retina.

scholarly journals Pre- and Postnatal Damage to the Retro-Geniculate Visual Pathways Cause Retinal Degeneration Predictive for Visual Function

2021 ◽  
Vol 15 ◽  
Author(s):  
Finn Lennartsson ◽  
HannaMaria Öhnell ◽  
Lena Jacobson ◽  
Maria Nilsson
Keyword(s):  
Visual System ◽  
Plexiform Layer ◽  
Visual Pathways ◽  
Research Report ◽  
Inner Plexiform Layer ◽  
Fiber Tractography ◽  
Fiber Layer ◽  
Teenagers And Young Adults ◽  
Magnetic Resonance Imaging Mri ◽  
And Function

To increase the understanding of the relationship between structure and function in individuals with damage to the brain from different stages of maturation of the visual system, we examined 16 teenagers and young adults. We used diffusion-weighted magnetic resonance imaging (MRI) and fiber tractography of the optic radiation (OR) and optical coherence tomography (OCT) of the peripapillary retinal nerve fiber layer (pRNFL) and the ganglion cell layer + inner plexiform layer (GC+IPL) in the macula. Visual field (VF) function was assessed with the Humphrey Field Analyzer (HFA). Injuries to the immature OR were associated with thinning of the pRNFL and GC+IPL, and corresponding VF defects irrespectively of timing of the lesion. However, in cases with bilateral white-matter damage of immaturity (WMDI) we noticed a well preserved central VF despite a very thin GC+IPL. We speculate that this is due to plasticity in the immature visual system. Similar results were not noticed among cases with unilateral damage, acquired pre- or postnatally, in which the central VF was affected in most cases. OCT has proved to be a valuable targeted tool in children with damage to the retro-geniculate visual pathways, and that focal thinning of the GC+IPL predicts VF defects. This brief research report includes a review of four previously published papers. In addition, we present one new case and apply a recently developed classification system for CVI. The classification was applied on cases with bilateral WMDI to investigate its relation to retinal structure.

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