scholarly journals Age-Related Alterations of Proteins in Albino Wistar Rat Retina

2021 ◽  
pp. 1-16
Author(s):  
Andrea Kovács-Valasek ◽  
Etelka Pöstyéni ◽  
Viktória Dénes ◽  
Adrienn Mester ◽  
György Sétáló Jr. ◽  
...  

Imbalance of homeostasis causes permanent changes in the body with time. The central nervous system is especially prone to these changes since it possesses limited regenerative capacity. In the retina, neurons are damaged during the aging process, and this eventually leads to deterioration of vision. In our 2-year-long study, we examined genetically closely related rat individuals to disclose the hidden retinal causes of age-associated visual dysfunction. Morphometric analysis showed significant reduction of the retina thickness with aging, particularly that of the inner plexiform layer. To reveal changes between the age groups, we used immunohistochemistry against vesicular glutamate transporter 1 protein for photoreceptor and bipolar cell terminals, Brn3a for ganglion cells, calbindin 28 kDa for horizontal cells, parvalbumin for AII amacrines, protein kinase Cα for rod bipolar cells, tyrosine hydroxylase for dopaminergic cells, glial fibrillary acidic protein for glial cells, and peanut-agglutinin labeling for cones. The most significant decrease was observed in the density of photoreceptor and the ganglion cells in the aging process. By using immunocytochemistry and western blot technique, we observed that calbindin and vesicular glutamate transporter 1 protein staining do not change much with aging; tyrosine hydroxylase, parvalbumin and calretinin showed the highest immunoreactivity during the midlife period. Most interestingly, the level of glial fibrillary acidic protein also changes similarly to the previously named markers. Our results provide further evidence that protein content is modified at least in some cell populations of the rat retina, and the number of retinal cells declined with aging. We conclude that senescence alone may cause structural and functional damage in the retinal tissue.

2015 ◽  
Vol 32 ◽  
Author(s):  
DAVID W. MARSHAK ◽  
ALICE Z. CHUANG ◽  
DREW M. DOLINO ◽  
ROY A. JACOBY ◽  
WEILEY S. LIU ◽  
...  

AbstractThe goals of these experiments were to describe the morphology and synaptic connections of amacrine cells in the baboon retina that contain immunoreactive vesicular glutamate transporter 3 (vGluT3). These amacrine cells had the morphology characteristic of knotty bistratified type 1 cells, and their dendrites formed two plexuses on either side of the center of the inner plexiform layer. The primary dendrites received large synapses from amacrine cells, and the higher-order dendrites were both pre- and postsynaptic to other amacrine cells. Based on light microscopic immunolabeling results, these include AII cells and starburst cells, but not the polyaxonal amacrine cells tracer-coupled to ON parasol ganglion cells. The vGluT3 cells received input from ON bipolar cells at ribbon synapses and made synapses onto OFF bipolar cells, including the diffuse DB3a type. Many synapses from vGluT3 cells onto retinal ganglion cells were observed in both plexuses. At synapses where vGluT3 cells were presynaptic, two types of postsynaptic densities were observed; there were relatively thin ones characteristic of inhibitory synapses and relatively thick ones characteristic of excitatory synapses. In the light microscopic experiments with Neurobiotin-injected ganglion cells, vGluT3 cells made contacts with midget and parasol ganglion cells, including both ON and OFF types. Puncta containing immunoreactive gephyrin, an inhibitory synapse marker, were found at appositions between vGluT3 cells and each of the four types of labeled ganglion cells. The vGluT3 cells did not have detectable levels of immunoreactive γ-aminobutyric acid (GABA) or immunoreactive glycine transporter 1. Thus, the vGluT3 cells would be expected to have ON responses to light and make synapses onto neurons in both the ON and the OFF pathways. Taken with previous results, these findings suggest that vGluT3 cells release glycine at some of their output synapses and glutamate at others.


2019 ◽  
Vol 33 (9) ◽  
pp. 775-784 ◽  
Author(s):  
Sohee Park ◽  
Cai-yue Liu ◽  
Patricia J. Ward ◽  
Poonam B. Jaiswal ◽  
Arthur W. English

One hour of 20-Hz continuous electrical stimulation (ES) applied at the time of injury promotes the regeneration of axons in cut peripheral nerves. A more robust enhancement of peripheral axon regeneration is achieved by 2 weeks of daily treadmill exercise. We investigated whether repeated applications of brief ES (mES) would be more effective in promoting regeneration than a single application. Sciatic nerves of C57B6 mice were cut and repaired by end-to-end anastomosis. At that time and every third day for 2 weeks, the repaired nerve was stimulated for 1 hour at 20 Hz. In controls, injured mice were either untreated or treated with ES only once. Direct muscle responses recorded from reinnervated muscles in awake animals were observed earlier both in mice treated with ES and mES than untreated controls. Their amplitudes increased progressively over the post transection study period, but the rate of this progression was increased significantly only in animals treated once with ES. Monosynaptic H reflexes recovered to pretransection levels in both untreated and singly treated mice but in the animals treated repeatedly, they were maintained at more than twice that of the same reflexes recorded prior to injury. In anatomical analyses, both excitatory and inhibitory synaptic contacts with the cell bodies of injured motoneurons, including those expressing the vesicular glutamate transporter 1 (VGLUT1), were sustained in mice treated repeatedly but not in singly treated or untreated mice. Repeated ES does not enhance the rate of restoration of functional muscle reinnervation and results in the retention of exaggerated reflexes.


2009 ◽  
Vol 25 (1) ◽  
pp. 25-39 ◽  
Author(s):  
CA Dodd ◽  
BG Klein

The pyrethroid insecticide permethrin and the organophosphate insecticide chlorpyrifos can experimentally produce Parkinson’s disease (PD)-associated changes in the dopaminergic nigrostriatal pathway, short of frank degeneration, although at doses considerably higher than from a likely environmental exposure. The ability of permethrin (200 mg/kg), chlorpyrifos (50 mg/kg), or combined permethrin + chlorpyrifos to facilitate nigrostriatal damage in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) (30 mg/kg) C57BL/6 mouse model of PD was investigated in three separate experiments. Tyrosine hydroxylase (TH) and glial fibrillary acidic protein (GFAP) immunohistochemistry assessed nigrostriatal degeneration or nigrostriatal damage more subtle than frank degeneration. Four fields in the dorsolateral caudate-putamen were examined at two rostrocaudal locations. The dopaminergic neurotoxin MPTP decreased striatal TH immunopositive neuropil and increased GFAP immunopositive neuropil. Neither permethrin nor chlorpyrifos, alone or in combination, altered the effects of MPTP upon TH or GFAP immunostaining. Permethrin alone increased striatal GFAP immunopositive neuropil but not when combined with chlorpyrifos treatment. Therefore, combined administration of the two insecticides appeared to protect against an increase in a neuropathological indicator of striatal damage seen with permethrin treatment alone. Differences compared with analysis of entire striatum emphasize the value of varying the topographic focus used to assess nigrostriatal degeneration in studies of insecticides in PD.


2008 ◽  
Vol 1215 ◽  
pp. 20-29 ◽  
Author(s):  
Salvatore L. Stella ◽  
Stefanie Li ◽  
Andrea Sabatini ◽  
Alejandro Vila ◽  
Nicholas C. Brecha

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