Cellular Decay in the Rat Retina During Normal Post-natal Development: A Preliminary Quantitative Analysis of the Basic Endogenous Rhythm

Vogel, Margarete; Möller, K. O.

doi:10.1007/978-3-642-81445-7_11

Cited by 4 publications

(5 citation statements)

References 25 publications

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“…However, at P21, SD rats exposed for 24 h showed a significant reduction (Student’s t ‐test, p < 0.001) in the ONL. An increase in the ONL thickness at P27 is observed in both unexposed SD and P23H rats, which is due to a developmentally controlled expansion of the photoreceptor layer in the third week of the rat development (Vogel and Möller 1980). However, 24 h light exposure at P20 caused a significant reduction in the ONL thickness of both SD and P23H rats at P27 (Student’s t ‐test, p < 0.05) (Fig.…”

Section: Resultsmentioning

confidence: 99%

Light exposure causes functional changes in the retina: increased photoreceptor cation channel permeability, photoreceptor apoptosis, and altered retinal metabolic function

Yu¹,

Acosta²,

Ready³

et al. 2007

Journal of Neurochemistry

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Light exposure induces retinal photoreceptor degeneration and retinal remodeling in both the normal rat retina and in animal models of retinal degeneration. Although cation entry is one of the triggers leading to apoptosis, it is unclear if this event occurs in isolation, or whether a number of pathways lead to photoreceptor apoptosis following light exposure. Following light exposure, we investigated the characteristics of cation entry, apoptotic markers [using terminal deoxynucleotidyl transferase (EC 2.7.7.31) dUTP nick-end labeling (TUNEL) labeling] and metabolic properties of retina from Sprague-Dawley (SD) rats and a rat model of retinitis pigmentosa [proline-23-histidine (P23H) rat]. Assessment of cation channel permeability using agmatine (AGB) labeling showed that excessive cation gating accompanied the series of anomalies that occur prior to photoreceptor loss. Increased AGB labeling in photoreceptors was seen in parallel with the appearance of apoptotic photoreceptors detected by TUNEL labeling with only a smaller proportion of cells colocalizing both markers. However, SD and P23H retinal photoreceptors differed in the amounts and colocalization of AGB gating and TUNEL labeling as a function of light exposure. Finally, reduced retinal lactate dehydrogenase levels were found in SD and P23H rat retinas after a 24-h light exposure period. Short-term (2 h) exposure of the P23H rat retina caused an increase in lactate dehydrogenase activity suggesting increased metabolic demand. These results suggest that energy availability may be exacerbated during the early stages of light exposure in susceptible retinas. Also, the concomitant observation of increased ion gating and TUNEL labeling suggest the existence of at least two possible mechanisms in light-damaged retinas in both SD and the P23H rat retina.

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Section: Resultsmentioning

confidence: 99%

Light exposure causes functional changes in the retina: increased photoreceptor cation channel permeability, photoreceptor apoptosis, and altered retinal metabolic function

Yu¹,

Acosta²,

Ready³

et al. 2007

Journal of Neurochemistry

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“…Thus, the first aim of our work was to provide a comprehensive kinetic analysis of apoptosis during the whole normal retinal development in the mouse. Considerable differences in the pattern of apoptosis have been reported between different individual animals at the same developmental stage (Vogel and Moller, 1980; Young, 1984; Portera‐Cailliau et al, 1994). To reduce this variability, we used congenic B6 mice that were killed at the same time of day and we counted the cells in several retinal sections from each animal.…”

Section: Discussionmentioning

confidence: 99%

Major role of BAX in apoptosis during retinal development and in establishment of a functional postnatal retina

Péquignot¹,

Provost²,

Salle³

et al. 2003

Developmental Dynamics

117

123

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Apoptosis plays a major role in the development of the central nervous system. Previous studies of apoptosis induction during retinal development are difficult to interpret, however, because they explored different mouse strains, different developmental periods, and used different assays. Here, we first established a comprehensive sequential pattern of cell death during the whole development of the C57BL/6J mouse retina, from E10.5 to postnatal day (P) 21 by using the terminal deoxynucleotidyl transferase (TdT) -mediated deoxyuridine triphosphate (dUTP)-biotinylated nick end labeling (TUNEL) assay. We confirmed the existence of three previously described apoptotic peaks and identified another, later peak at P15, in both the outer nuclear layer, in which the photoreceptors differentiate, and the ganglion cell layer. Comparison of wild-type C57BL/6 mice, gld mice, defective in the death ligand fasL, and bax-/-mice, defective in the pro-apoptotic BAX protein, revealed a minor role for FAS ligand but a crucial role for BAX in both apoptosis and normal retinal development. The lack of BAX resulted in thicker than normal inner neuroblastic and ganglion cell layers in adults, with larger numbers of cells and an impaired electroretinogram response related to a decreased number of responsive cells. Our findings indicate that cell death during normal retinal development is important for the modeling of a functional vision organ and showed that the pro-apoptotic BAX protein plays a crucial role in this process. Developmental Dynamics 228:231-238, 2003.

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“…However, amacrine cell death does not cease until day 26 and bipolar cell degeneration continues for 48 days. With respect to photoreceptor cell death, a second phase of apoptosis has been reported between days 12 and 72, peaking at P23 (Vogel and Möller, 1980). Cell death in the mouse retina occurs primarily during the first 2 weeks after birth and is essentially completed by the end of the third week.…”

Section: Rodentsmentioning

confidence: 99%

“…Further studies using the retina will help to completely characterize the complex processes underlying cell death. Timing of retinal cell Apoptosis in the different layers of the retina in zebrafish (Biehlmaier et al, 2001), Xenopus (Gaze and Grant, 1992), chicken (García-Porrero and Ojeda, 1979;Cuadros andRíos, 1988, Cook et al, 1998), rat (Vogel and Möller, 1980;Galli-Resta and Ensini, 1996), mouse (Young, 1984), and human Georges et al, 1999) during retinal development. Abbreviations: AC, amacrine cells; d, days; dpf, days post-fertilization; E, embryonic day; GCL, ganglion cell layer; h, hours; hpf, hours post-fertilization; INL, inner nuclear layer; MC, Müller cells; ONL, outer nuclear layer; P, postnatal; wg, weeks of gestation.…”

Section: Concluding Commentsmentioning

confidence: 99%

Cell death in the developing vertebrate retina

Vecino¹,

Hernández²,

Garcı́a³

2004

Int. J. Dev. Biol.

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Programmed cell death occurs naturally, as a physiological process, during the embryonic development of multicellular organisms. In the retina, which belongs to the central nervous system, at least two phases of cell death have been reported to occur during development. An early phase takes place concomitant with the processes of neurogenesis, cell migration and cell differentiation. A later phase affecting mainly neurons occurs when connections are established and synapses are formed, resulting in selective elimination of inappropriate connections. This pattern of cell death in the developing retina is common among different vertebrates. However, the timing and magnitude of retinal cell death varies among species. In addition, a precise regulation of apoptosis during retinal development has been described. Factors such as neurotrophins, among many others, and electrical activity influence the survival of retinal cells during the course of development. In this paper, we present a summary of these different aspects of programmed cell death during retinal development, and examine how these differ among different species.

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Cellular Decay in the Rat Retina During Normal Post-natal Development: A Preliminary Quantitative Analysis of the Basic Endogenous Rhythm

Cited by 4 publications

References 25 publications

Light exposure causes functional changes in the retina: increased photoreceptor cation channel permeability, photoreceptor apoptosis, and altered retinal metabolic function

Light exposure causes functional changes in the retina: increased photoreceptor cation channel permeability, photoreceptor apoptosis, and altered retinal metabolic function

Major role of BAX in apoptosis during retinal development and in establishment of a functional postnatal retina

Cell death in the developing vertebrate retina

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