Pattern-reversal retinal potentials(PRRP) are electrical signals generated within retina, possibly by the retinal ganglion cells, when a phase-alternating check board pattern is viewed. Authors clinically studied the characteristics of PRRP the mean amplitude and latency with 24 minute checks, the effect of the spatial frequency, the effect of defocusing and the retinocortical time in 20 normals, using Nicolet CA 1,000. The results are as follows; 1. The mean latency P1 and the mean P1-N2 amplitude of PRRP in normal group was 39.19 +/- 3.30(msec), 1.32 +/- 0.22(uV), respectively. 2. The mean retinocortical time in normal group was 52.93 +/- 7.39(msec). 3. The P1-N2 amplitude of PRRP was reduced linearly with increasing defocusing, and significant amplitude reduction was observed when defocusing amounted to +1D. 4. When central 3 degree of stimulus was covered in order to simulate a macular pathology, PRRP to 24 minute checks was abnormal both in amplitude and latency. 5. Peak response amplitude of PRRP was obtained with large checksizes(3 degrees 12 minutes, 6 degrees 24 minutes).
Pathology ; Retina ; Retinal Ganglion Cells ; Retinaldehyde*

In order to elucidate in vivo neuronal cell death in the retina, and involvement of NF-kappa B in this process, we studied the degeneration of retinal ganglion cells (RGCs) and the activation of NF-kappa B after transection of the optic nerve of adult rat at 5 mm from the eyeball. The morphology of dying ganglion cells in the retinal ganglion cell layer was observed by light and electron microscopy, the activation of NF-kappa B was investigated immunohistochemically. Seven and 14 days post-axotomy, dying cells contained pyknotic nuclei. The death of retinal ganglion cells involved apoptosis, activation of NF-kappa B (p50 and p65) was prominent in a time dependent manner. We observed axotomy-induced NF-kappa B activation, which may mediate apoptosis of retinal ganglion cells.
Animal ; Apoptosis/physiology ; Axotomy ; Immunohistochemistry ; Male ; Microscopy, Electron ; NF-kappa B/biosynthesis* ; Optic Nerve/surgery ; Rats ; Rats, Sprague-Dawley ; Retinal Ganglion Cells/ultrastructure ; Retinal Ganglion Cells/pathology* ; Retinal Ganglion Cells/metabolism ; Substances: NF-kappa B

OBJECTIVETo gain insight into the potential mechanism of mitochondria dysfunction in pathogenesis, progression and therapeutic management of glaucoma.

DATA SOURCESThe data used in this review were mainly published in English from 2000 to present obtained from PubMed. The search terms were "mitochondria", "glaucoma" and "trabecular meshwork" or "retinal ganglion cells".

STUDY SELECTIONArticles studying the mitochondria-related pathologic mechanism and treatment of glaucoma were selected and reviewed.

RESULTSMitochondrial dysfunction or injury was demonstrated in different eye tissue of glaucoma. A variety of potential injuries (light, toxic materials, oxidative injury, mechanical stress, aging, etc.) and the inherent DNA defects are deemed to cause mitochondrial structural and functional destruction in trabecular meshwork cells, retinal ganglion cells, etc. of glaucoma. In addition, various new experimental and therapeutic interventions were used to preserve mitochondrial function, which may be useful for protecting against optic nerve degeneration or reducing the death of retinal ganglion cells in glaucoma.

CONCLUSIONSMitochondria play an important role in the pathogenesis of glaucoma, various strategies targeting mitochondrial protection might provide a promising way to delay the onset of glaucoma or protect RGCs against glaucomatous damage.

Glaucoma ; metabolism ; pathology ; Humans ; Mitochondria ; metabolism ; Retinal Ganglion Cells ; metabolism ; Trabecular Meshwork ; metabolism

BACKGROUNDTraumatic optic neuropathy (TON) is one of the reasons for permanent vision loss. Currently, the clinical practices may not be sufficient for direct assessments and comprehensively determining the location and extent of the patients with optic nerve injury in traumatic optic neuropathy. Magnetic resonance imaging (MRI) provides a non-invasive option. However, rare reports have found whether the differentdegree of injury of the optic nerve can be detected by manganese-enhanced MRI (MEMRI). This study aimed to explore the efficacy of MEMRI in the visual pathway for different severity of opitic nerve injury in rats.

METHODSThe different injuries of mild, moderate, and heavy damages were created by modified reverse tweezer and were evaluated by counting retinal ganglion cells (RGCs) and VEP ananlysis. Sprague-Dawley (SD) rats were intravitreally injected with 2 l of 25 mmol/L MnCl2, which has been confirmed as a safe injection concentration. The contrast-to-noise ratio (CNR) of MEMRI for optic nerve enhancement at different injury levels was measured.

RESULTSThe location of the significantly decreased signal point on optic nerve (ON) was corresponding to the location we made. However, similar findings are not obvious, or even have not been observed in 28 days in each group and also in 14 days at F100 group, indicating that MEMRI could be directly intuitive positioned in the early stage on the optic nerve injury.

CONCLUSIONSThe possibility of using MEMRI in optic nerve injury in a safe injection concentration of 25 mmol/L is confirmed. Therefore, it is possible to detect the severity of the optic nerve by MEMRI examination.

Animals ; Magnetic Resonance Imaging ; methods ; Male ; Manganese ; Optic Nerve Injuries ; diagnosis ; pathology ; Rats ; Rats, Sprague-Dawley ; Retinal Ganglion Cells ; pathology

BACKGROUNDGlaucoma can cause progressive damage to retinal ganglion cells. These cells can be classified as cells projecting to the superior colliculus and melanopsin-containing retinal ganglion cells, which project to the suprachiasmatic nucleus. This study was to investigate the effects of chronic intraocular pressure elevation on melanopsin-containing retinal ganglion cells in rats.

METHODSChronic intraocular pressure elevation was induced in one eye of adult Wistar rats by cauterization of three episcleral veins. Intraocular pressure was measured at different intervals with a rebound tonometer. Superior collicular retinal ganglion cells were retrogradely labeled from the superior colliculus with Fluorogold. Melanopsin-containing retinal ganglion cells were visualized by free-floating immunohistochemistry on whole-mount retinas. The number of labeled superior collicular and melanopsin-containing retinal ganglion cells were counted in the sample areas on flat-mounted retinas.

RESULTSCompared with contralateral control eyes, the numbers of both superior collicular and melanopsin-containing retinal ganglion cells were significantly reduced after 12 weeks of experimental intraocular pressure elevation ((2317.41 +/- 29.96)/mm(2) vs (1815.82 +/- 24.25)/mm(2); (26.20 +/- 2.10)/mm(2) vs (20.62 +/- 1.52)/mm(2), respectively). The extent of cell loss of the two types of retinal ganglion cells was similar. However, no morphologic changes were found in melanopsin-containing retinal ganglion cells.

CONCLUSIONBoth melanopsin-containing and superior collicular retinal ganglion cells were damaged by chronic ocular hypertension, indicating that glaucomatous neural degeneration involves the non-image-forming visual pathway.

Animals ; Disease Models, Animal ; Glaucoma ; pathology ; Intraocular Pressure ; Male ; Rats ; Rats, Wistar ; Retinal Ganglion Cells ; pathology ; Rod Opsins ; analysis

Diabetic Retinopathy ; complications ; epidemiology ; physiopathology ; Humans ; Neurodegenerative Diseases ; epidemiology ; etiology ; physiopathology ; Retinal Ganglion Cells ; pathology ; Risk Factors

PURPOSE: This study was designed to assess and compare the thicknesses of the fovea and the retinal nerve fiber layer in normal children and children with amblyopia. METHODS: Optical Coherence Tomography (OCT) was performed on 26 children (52 eyes total) with unilateral amblyopia that was due to anisometropia or strabismus. OCT was also performed on 42 normal children (84 eyes), for a total of 136 eyes. Retinal thickness measurements were taken from the fovea, and the retinal nerve fiber layer thickness measurements were taken from the superior, inferior, nasal and temporal quadrants in the peripapillary region. RESULTS: The average age of the normal children was 8.5 years, and the average age of the children with amblyopia was 8.0 years. The average thickness of the fovea was 157.4 micrometer in normal eyes and was 158.8 micrometer in amblyopic eyes. The difference between the two groups was not statistically significant (p=0.551). The thicknesses of the superior, inferior, nasal and temporal quadrants of the retinal nerve fiber layer between the normal children and the children with amblyopia were also not statistically significant (p=0.751, 0.228, 0.696 and 0.228, respectively). However, for the children with anisometropic amblyopia and the children with strabismic amblyopia, the average thicknesses of the fovea were 146.5 micrometer and 173.1 micrometer, respectively, and the retinal nerve fiber layer thicknesses were measured to be 112.9 micrometer and 92.8 micrometer, respectively, and these were statistically significant differences (p=0.046, 0.034, respectively). CONCLUSIONS: Normal thicknesses of the fovea and the retinal nerve fiber layers were established, and there were no differences in the fovea and the retinal nerve fiber layer thickness found between normal children and children with amblyopia.
Tomography, Optical Coherence ; Severity of Illness Index ; Retrospective Studies ; Retinal Ganglion Cells/*pathology ; Nerve Fibers/*pathology ; Male ; Humans ; Fovea Centralis/*pathology ; Female ; Child, Preschool ; Child ; Amblyopia/*pathology ; Adolescent

PURPOSE: To evaluate the effect of axial length on the variability of retinal nerve fiber layer (RNFL) thickness measurements using the Stratus optical coherence tomography (OCT) in normal and glaucomatous eyes. METHODS: We measured the RNFL thickness in 474 subjects using the Stratus OCT twice during the same day. Axial length was measured with the IOLMaster, and refractive error was the absolute value of the spherical equivalent measured with an auto ref-keratometer. Standard deviation in overall mean RNFL thickness was used as the dependent variable to identify significant correlations. RESULTS: Long axial length affected the variability in the RNFL thickness value by stratus OCT at the temporal quadrant (p = 0.006) and clock-hour sector 9 (p = 0.001). Refractive error also affected the variability of the RNFL thickness value by stratus OCT at the temporal quadrant (p = 0.025) and clock-hour sector 9 (p = 0.024). CONCLUSIONS: It is clinically significant that longer axial length demonstrates greater variability in temporal area as detected by OCT, a measurement which correlates with the preferably damaged position in the myopic glaucoma eye.
Adult ; Aged ; Female ; Glaucoma/*pathology ; Humans ; Male ; Middle Aged ; Myopia, Degenerative/*pathology ; Nerve Fibers/*pathology ; Prospective Studies ; Refractive Errors ; Retinal Ganglion Cells/*pathology ; Tomography, Optical Coherence/*methods

A 59-year-old woman was referred to our clinic for a glaucoma evaluation. The visual acuity and intraocular pressure were normal in both eyes. However, red-free fundus photography in the left eye showed a superotemporal wedge-shaped retinal nerve fiber layer defect, and visual field testing showed a corresponding partial arcuate scotoma. In an optical coherence tomography examination, the macula was flat, but an arcuate-shaped peripapillary retinoschisis was found. Further, the retinoschisis seemed to be connected with a superotemporal optic pit shown in a disc photograph. After 3 months of a topical prostaglandin analogue medication, the intraocular pressure in the retinoschisis eye was lowered from 14 to 10 mmHg and the peripapillary retinoschisis was almost resolved. We report a rare case of an optic disc pit with peripapillary retinoschisis presenting as a localized retinal nerve fiber layer defect.
Female ; Humans ; Middle Aged ; Nerve Fibers/*pathology ; Optic Disk/*abnormalities/*pathology ; Optic Nerve Diseases/*diagnosis ; Retinal Ganglion Cells/*pathology ; Retinoschisis/*diagnosis/drug therapy ; Tomography, Optical Coherence

OBJECTIVETo investigate the injury effects of microwave on the visual performance and the apoptosis of retinal ganglion cells (RGCs) in rats and the relationship between the impaired visual performance and RGCs apoptosis induced by microwave.

METHODSThe visual performance of rats was observed by Electroretinogram (ERG) and Flash visual evoked potentials (F-VEP). The apoptosis of RGCs in vivo and in vitro was detected by TUNEL assay and Hoechst staining.

RESULTSMicrowave exposure had no influence on ERG-a wave. The amplitude of ERG-b wave decreased significantly on the 3rd day and 7th day after microwave exposure (P < 0.01).The latency of ERG-b wave shortened significantly only at 3rd day after microwave exposure (P < 0.01). The latency of F-VEP extended markedly on the 3rd day after exposure (P < 0.05) and recovered on the 7th day after microwave exposure. The amplitude of F-VEP decreased significantly in exposure group, as compared with sham-exposure group, on the 3rd day and 7th day after microwave exposure (P < 0.05). After microwave exposure for 12 h, the apoptotic rate of RGCs in rat increased from 2.85% to 6.73%, and on the 7th day after exposure, the apoptotic rate of RGCs remained 8.93% (P < 0.05). The apoptotic rate of cultured RGCs increased from 8.42% to 13.91% at 6 hour (P < 0.05) and to 24.14% at 24 hour (P < 0.01) after microwave exposure (P < 0.05 or P < 0.01).

CONCLUSIONMicrowave exposure can injure the visual performance of rats, and the apoptosis of RGCs induced microwave may be one of the main pathological mechanisms.

Animals ; Apoptosis ; radiation effects ; Cells, Cultured ; Male ; Microwaves ; adverse effects ; Rats ; Rats, Sprague-Dawley ; Retina ; radiation effects ; Retinal Ganglion Cells ; pathology ; radiation effects