scholarly journals Analysis of Programmed Cell Death and Senescence Markers in the Developing Retina of an Altricial Bird Species

Cells ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 504
Author(s):  
Guadalupe Álvarez-Hernán ◽  
José Antonio de Mera-Rodríguez ◽  
Ismael Hernández-Núñez ◽  
Alfonso Marzal ◽  
Yolanda Gañán ◽  
...  

This study shows the distribution patterns of apoptotic cells and biomarkers of cellular senescence during the ontogeny of the retina in the zebra finch (T. guttata). Neurogenesis in this altricial bird species is intense in the retina at perinatal and post-hatching stages, as opposed to precocial bird species in which retinogenesis occurs entirely during the embryonic period. Various phases of programmed cell death (PCD) were distinguishable in the T. guttata visual system. These included areas of PCD in the central region of the neuroretina at the stages of optic cup morphogenesis, and in the sub-optic necrotic centers (St15–20). A small focus of early neural PCD was detected in the neuroblastic layer, dorsal to the optic nerve head, coinciding with the appearance of the first differentiated neuroblasts (St24–St25). There were sparse pyknotic bodies in the non-laminated retina between St26 and St37. An intense wave of neurotrophic PCD was detected in the laminated retina between St42 and P8, the last post-hatching stage included in the present study. PCD was absent from the photoreceptor layer. Phagocytic activity was also detected in Müller cells during the wave of neurotrophic PCD. With regard to the chronotopographical staining patterns of senescence biomarkers, there was strong parallelism between the SA-β-GAL signal and p21 immunoreactivity in both the undifferentiated and the laminated retina, coinciding in the cell body of differentiated neurons. In contrast, no correlation was found between SA-β-GAL activity and the distribution of TUNEL-positive cells in the developing tissue.

1999 ◽  
Vol 44 ◽  
pp. S74-S84 ◽  
Author(s):  
Hidehiro Oku ◽  
Tetsuya Sugiyama ◽  
Shota Kojima ◽  
Toshio Watanabe ◽  
Ikuo Azuma

2005 ◽  
Vol 171 (2) ◽  
pp. 313-325 ◽  
Author(s):  
Tatjana C. Jakobs ◽  
Richard T. Libby ◽  
Yixin Ben ◽  
Simon W.M. John ◽  
Richard H. Masland

Using a variety of double and triple labeling techniques, we have reevaluated the death of retinal neurons in a mouse model of hereditary glaucoma. Cell-specific markers and total neuron counts revealed no cell loss in any retinal neurons other than the ganglion cells. Within the limits of our ability to define cell types, no group of ganglion cells was especially vulnerable or resistant to degeneration. Retrograde labeling and neurofilament staining showed that axonal atrophy, dendritic remodeling, and somal shrinkage (at least of the largest cell types) precedes ganglion cell death in this glaucoma model. Regions of cell death or survival radiated from the optic nerve head in fan-shaped sectors. Collectively, the data suggest axon damage at the optic nerve head as an early lesion, and damage to axon bundles would cause this pattern of degeneration. However, the architecture of the mouse eye seems to preclude a commonly postulated source of mechanical damage within the nerve head.


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