Aging Rat Vestibular Ganglion: II. Quantitative Electron Microscopic Evaluation

1997 ◽  
Vol 106 (9) ◽  
pp. 753-758 ◽  
Author(s):  
Michael J. Lyon ◽  
Jeffrey M. King
Keyword(s):  
Golgi Apparatus ◽  
Ganglion Cell ◽  
Ganglion Cells ◽  
Cell Loss ◽  
Wistar Rat ◽  
Electron Microscopic ◽  
Vestibular Ganglion ◽  
Age Related ◽  
Microscopic Evaluation ◽  
Change In Mean

This laboratory has shown that age-related vestibular ganglion cell loss does not occur in the Wistar rat as it does in humans. However, in that study, intracellular changes were evident. The purpose of the present study was to quantitate some of these changes. The volume densities of mitochondria, rough endoplasmic reticulum (RER), Golgi apparatus, and aging pigment, as well as the diameter of the vestibular ganglion cells, of young (3 to 5 months) and old (24 to 31 months) female Wistar rats were determined by electron microscopy and stereological techniques. The data show a significant decrease in the volume densities of mitochondria (11.4%), Golgi apparatus (8.1%), and RER (8.9%), a significant increase in aging pigment (327%), and no change in mean profile diameter. These results suggest a decreased capacity for oxidative metabolism and protein synthesis that may reflect a decrease in the number of hair cells innervated by each ganglion cell and/or in the number of central connections. In either case, these findings suggest impaired metabolic and functional capabilities.

Scanning Electron Microscopic Evaluation of Age-Related Changes in the Rat Vestibular Epithelium

1994 ◽  
Vol 111 (6) ◽  
pp. 799-806 ◽  
Author(s):  
Meiho Nakayama ◽  
Robert H. Helfert ◽  
Horst R. Konrad ◽  
Donald M. Caspary
Keyword(s):  
Hair Cells ◽  
Vestibular Function ◽  
Fischer 344 Rats ◽  
Human Beings ◽  
Electron Microscopic ◽  
Fischer 344 ◽  
Age Related ◽  
Microscopic Evaluation ◽  
Age Related Changes ◽  
Scanning Electron

An ultrastructural study was performed to assets age-related changes in the vestibular end organs of Fischer 344 rats. The surfaces of the maculae and cristae from 3-, 12-, and 24-month-old Fischer 344 rats were observed by use of scanning electron microscopy. Age-related changes in the morphology of the vestibular neuroepithelium included a substantial loss of hair cells, as well as a reduction in the number of kinocllia and stereocilla on those that remained. These changes were greatest in the central upper regions of the three ampullae. In aged animals a greater area of the neuroepithelial surface was covered with microvilli, and in some instances, giant cilia were found among the microvillous surfaces. In contrast, there were few differences among the three age groups in the number and condition of hair cells in the saccules and utricles. The changes observed in the cristae may contribute to the age-associated impairment of vestibular function. If similar changes occur in human beings, these could in part account for the presbycusis observed in the elderly.

scholarly journals mTOR-dependent dysregulation of autophagy contributes to the retinal ganglion cell loss in streptozotocin-induced diabetic retinopathy

2020 ◽  
Author(s):  
Sanjar Batirovich Madrakhimov ◽  
Jin Young Yang ◽  
Jin Ha Kim ◽  
Jung Woo Han ◽  
Tae Kwann Park
Keyword(s):  
Diabetic Retinopathy ◽  
Ganglion Cell ◽  
Ganglion Cells ◽  
Neuronal Cell ◽  
Cell Loss ◽  
Retinal Ganglion ◽  
Diabetic Mice ◽  
Tissue Samples ◽  
Glucose Transporter 1 ◽  
Apoptosis Pathway

Abstract Background: Neurodegeneration, an early event in the pathogenesis of diabetic retinopathy (DR), precedes clinically detectable microvascular damage. Autophagy dysregulation is considered a potential cause of neuronal cell loss, however underlying mechanisms remain unclear. The mechanistic target of rapamycin (mTOR) integrates diverse environmental signals to coordinate biological processes, including autophagy. Here, we investigated the role of mTOR signaling in neuronal cell death in diabetic retinopathy. Methods: Diabetes was induced by a single intraperitoneal injection of streptozotocin and tissue samples were harvested at 1, 2, 3, 4, and 6 months of diabetes. Early-stage of diabetic retinopathy was investigated in 1-month-diabetic mice treated with phlorizin or rapamycin. The effect of autophagy modulation on retinal ganglion cells was investigated in 3-months-diabetic mice treated with phlorizin or MHY1485. Tissue samples obtained from treated/untreated diabetic mice and age-matched controls were used for Western blot and histologic analysis.Results: mTOR-related proteins and glucose transporter 1 (GLUT1) was upregulated at 1 month and downregulated in the following period up to 6 months. Diabetes-induced neurodegeneration was characterized by an increase of apoptotic marker – cleaved caspase 3, a decrease of the total number of cells, and NeuN immunoreactivity in the ganglion cell layer (GCL), as well as an increase of autophagic protein. Insulin-independent glycemic control restored the mTOR pathway activity and GLUT1 expression, along with a decrease of autophagic and apoptotic proteins in 3-months-diabetic mice neuroretina. However, blockade of autophagy using MHY1485 resulted in a more protective effect on ganglion cells compared with phlorizin treatment. Conclusion: Collectively, our study describes the mechanisms of neurodegeneration through the hyperglycemia/ mTOR/ autophagy/ apoptosis pathway.

Light and Electron Microscopic Features of the Rat Vestibular Ganglion Cells

1993 ◽  
Vol 113 (sup503) ◽  
pp. 132-135 ◽  
Author(s):  
Kenji Okami ◽  
Toru Sekitani ◽  
Hiroshi Yasmashita ◽  
Yoichi Masumitsu
Keyword(s):  
Ganglion Cells ◽  
Electron Microscopic ◽  
Vestibular Ganglion ◽  
Microscopic Features ◽  
Vestibular Ganglion Cells

Monocular enucleation prevents retinal ganglion-cell loss following neonatal visual cortex damage in cats

1998 ◽  
Vol 15 (6) ◽  
pp. 1097-1105 ◽  
Author(s):  
KURT R. ILLIG ◽  
VON R. KING ◽  
PETER D. SPEAR
Keyword(s):  
Visual Cortex ◽  
Ganglion Cell ◽  
Ganglion Cells ◽  
Cell Loss ◽  
Dorsal Lateral Geniculate Nucleus ◽  
Medium Size ◽  
Retinal Ganglion ◽  
Retrograde Degeneration ◽  
Monocular Enucleation ◽  
Binocular Interactions

Damage to primary visual cortex (VC) in young cats leads to severe retrograde degeneration of the dorsal lateral geniculate nucleus (dLGN) and selective transneuronal retrograde degeneration of a class of retinal ganglion cells (RGCs) that have a medium-size soma. Previous studies have shown that “programmed” RGC death associated with normal development in one eye can be attenuated by removal of the other eye, suggesting that binocular interactions can influence developmental RGC death. The present study investigated whether removal of one eye also attenuates the ganglion cell loss that accompanies an early VC lesion. Five one-week-old cats received a unilateral VC lesion (areas 17, 18, and 19), and three of these cats also underwent monocular enucleation at the same time. Two normal control animals also were examined. RGC measurements were made from flat-mounted retinae when the animals were 5 weeks old. Sampling was restricted to a retinal area corresponding to the retinotopic representation included in the VC lesion. Results indicate that there is a marked loss of medium-size RGCs in the hemiretinae projecting to the damaged hemisphere in cats that received a VC lesion alone. However, there is no such loss in VC-lesion animals that also have a monocular enucleation. These results indicate that the transneuronal RGC loss that occurs after an early visual cortex lesion can be influenced by binocular interactions.

Rate of Quantal Excitation to a Retinal Ganglion Cell Evoked by Sensory Input

2000 ◽  
Vol 83 (5) ◽  
pp. 2956-2966 ◽  
Author(s):  
Michael A. Freed
Keyword(s):  
Ganglion Cell ◽  
Sensory Input ◽  
Ganglion Cells ◽  
Sustained Response ◽  
Alpha Cell ◽  
Fluctuation Analysis ◽  
Integration Interval ◽  
Response Component ◽  
Poisson Arrival ◽  
Change In Mean

To determine the rate and statistics of light-evoked transmitter release from bipolar synapses, intracellular recordings were made from on-alpha ganglion cells in the periphery of the intact, superfused, cat retina. Sodium channels were blocked with tetrodotoxin to prevent action potentials. A light bar covering the receptive field center excited the bipolar cells that contact the alpha cell and evoked a transient then a sustained depolarization. The sustained depolarization was quantified as change in mean voltage (Δ v), and the increase in voltage noise that accompanied it was quantified as change in voltage variance (Δς2). As light intensity increased, Δ v and Δς2 both increased, but their ratio held constant. This behavior is consistent with Poisson arrival of transmitter quanta at the ganglion cell. The response component attributable to glutamate quanta from bipolar synapses was isolated by application of 6-cyano-7-nitroquinoxaline (CNQX). As CNQX concentration increased, the signal/noise ratio of this response component (Δ v CNQX/ΔςCNQX) held constant. This is also consistent with Poisson arrival and justified the application of fluctuation analysis. Two different methods of fluctuation analysis applied to Δ v CNQX and ΔςCNQX produced similar results, leading to an estimate that a just-maximal sustained response was caused by ∼3,700 quanta s−1. The transient response was caused by a rate that was no more than 10-fold greater. Because the on-alpha cell at this retinal locus has ∼2,200 bipolar synapses, one synapse released ∼1.7 quanta s−1 for the sustained response and no more than 17 quanta s−1 for the transient. Consequently, within the ganglion cell's integration interval, here calculated to be ∼16 ms, a bipolar synapse rarely releases more than one quantum. Thus for just-maximal sustained and transient depolarizations, the conductance modulated by a single bipolar cell synapse is limited to the quantal conductance (∼100 pS at its peak). This helps preserve linear summation of quanta. The Δ v/Δς2ratio remained constant even as the ganglion cell's response saturated, which suggested that even at the peak of sensory input, summation remains linear, and that saturation occurs before the bipolar synapse.

scholarly journals Article Commentary: Retinal Ganglion Cell Loss in Diabetes Associated with Elevated Homocysteine

2009 ◽  
Vol 1 ◽  
pp. OED.S3417 ◽  
Author(s):  
Kenneth S. Shindler
Keyword(s):  
Ganglion Cell ◽  
Retinal Ganglion Cell ◽  
Ganglion Cell Layer ◽  
Ganglion Cells ◽  
Cell Layer ◽  
Cell Loss ◽  
Diabetic Patients ◽  
Retinal Ganglion ◽  
Heterozygous Deletion ◽  
Retinal Pathology

A number of studies have suggested that homocysteine may be a contributing factor to development of retinopathy in diabetic patients based on observed correlations between elevated homocysteine levels and the presence of retinopathy. The significance of such a correlation remains to be determined, and potential mechanisms by which homocysteine might induce retinopathy have not been well characterized. Ganapathy and colleagues 1 used mutant mice that have endogenously elevated homocysteine levels due to heterozygous deletion of the cystathionine-β-synthase gene to examine changes in retinal pathology following induction of diabetes. Their finding that elevated homocysteine levels hastens loss of cells in the retinal ganglion cell layer suggests that toxicity to ganglion cells may warrant further investigation as a potential mechanism of homocysteine enhanced susceptibility to diabetic retinopathy.

No age-related cell loss in three retinal nuclear layers of the Long-Evans rat

2007 ◽  
Vol 24 (6) ◽  
pp. 799-803 ◽  
Author(s):  
LIXIA FENG ◽  
ZHAOXIA SUN ◽  
HUI HAN ◽  
YIFENG ZHOU ◽  
MING ZHANG
Keyword(s):  
Ganglion Cell Layer ◽  
Ganglion Cells ◽  
Cell Layer ◽  
Outer Nuclear Layer ◽  
Photoreceptor Cells ◽  
Cell Loss ◽  
Related Cell ◽  
Age Related ◽  
Long Evans ◽  
Number Of Cells

The retina mainly contains ganglion, bipolar and photoreceptor cells which are distributed in the ganglion cell layer (GCL), inner nuclear layer (INL) and outer nuclear layer (ONL), respectively. Whether there is an age-related loss of these retinal cells remains not well understood. Cell density and the total number of cells were two commonly used measures to evaluate such age-related changes in most previous studies and provided controversial conclusions. The use of density measures as decisive data is problematic because the total area of the retina was expanded in aging, whereas the application of the total number of cells was limited for assessing ganglion cells. In this study, thus, we wanted to test whether there is an age-related cell loss in the GCL, INL and ONL and if so, whether such a loss is correlated to the convergence ratio of these cells. We used stereological procedures to quantify the total number of cells in the three retinal nuclear layers in six young and six aged Long-Evans rats. We found that during aging, the total volume of the retina remained unchanged, but the retina became thinner. There was no cell loss in each individual nuclear layer, and the ratio of the ONL to INL to GCL was preserved.

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