Structural and Functional Consequences of Trolox C Treatment in the Rat Model of Postnatal Hyperoxia

Dorfman, Allison; Dembinska, Olga; Chemtob, Sylvain; Lachapelle, Pierre

doi:10.1167/iovs.05-0727

Cited by 19 publications

(31 citation statements)

References 27 publications

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“…There are reports of impaired retinal function in OIR rodents (Akula et al 2007b;Dorfman et al 2006;Lachapelle et al 1999;Liu et al 2006a, b;Martini et al 2011;Narayanan et al 2011;Vessey et al 2011;Wilkinson-Berka et al 2010) and human ROP (for references, see Fulton et al 2009). These studies have shown decreased amplitude of the a-, bwaves and OPs, suggesting that both photoreceptors and post-receptor retina are affected by hypoxia.…”

Section: Electroretinographic Responses and Hypoxia Effectsmentioning

confidence: 99%

“…In addition, several glutamate antagonists along with free radical scavengers all reduce the ischemia-induced depression of the b-wave in rats (for references, see Block and Schwarz 1998). Moreover, a water-soluble analogue of vitamin E enhances the reduced b-wave and OPs in OIR rats (Dorfman et al 2006), whereas β2-adrenergic receptor blockade is effective in recovering electroretinographic responses in OIR mice .…”

Section: Sst 2 Role In Retinal Functionmentioning

confidence: 99%

“…In particular, the a-wave, which directly reflects photoreceptor responses to light, the b-wave, which is produced by second-order bipolar cells, and the oscillatory potentials (OPs), which are generated in the inner retina and reflect activities of inhibitory feedback circuits in the inner plexiform layer, all are reduced in OIR rodents (Akula et al 2007b;Dorfman et al 2006;Lachapelle et al 1999;Liu et al 2006a, b;Martini et al 2011;Narayanan et al 2011;Vessey et al 2011;Wilkinson-Berka et al 2010).…”

Section: Introductionmentioning

confidence: 99%

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Protective role of somatostatin receptor 2 against retinal degeneration in response to hypoxia

Monte

Latina

Cupisti

et al. 2012

Naunyn-Schmiedeberg's Arch Pharmacol

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In mouse retinal explants, octreotide, a somatostatin [somatotropin release-inhibiting factor (SRIF)] receptor 2 (sst(2)) agonist, prevents the hypoxia-induced vascular endothelial growth factor upregulation. In mice with oxygen-induced retinopathy (OIR), a model of retinopathy of prematurity, either sst(2) overexpression or octreotide have been found to limit hypoxia-induced angiogenic processes. Here, we investigated whether sst(2) influences retinal degeneration in response to hypoxia in wild-type (WT), sst(1)- and sst(2)-knockout (KO) mice. In retinal explants, we determined the role of sst(2) on apoptotic signals. In control condition, caspase-3 activity and the Bax/Bcl-2 ratio were lower in sst(1)-KO than in WT, but higher in sst(2)-KO than in WT retinas. In all strains, a comparable increase in caspase-3 activity and the Bax/Bcl-2 ratio was observed after hypoxia. The hypoxia-induced increase in apoptotic signals was recovered by octreotide in both WT and sst(1)-KO retinas. To investigate the role of sst(2) on retinal function, we recorded electroretinogram (ERG) in response to light flashes in OIR mice. ERG responses did not differ between WT and KO mice with the exception of oscillatory potentials (OPs) which, in sst(1)-KO mice, displayed much larger amplitude. In all strains, hypoxia drastically reduced a-, b-waves and OPs. In both WT and sst(1)-KO mice, octreotide recovered a- and b-waves, but did not recover OPs in sst(1)-KO mice. Neither apoptotic signals nor ERG was affected by octreotide in sst(2)-KO mice. These results show that sst(2) may protect retinal cells from hypoxia, thus implementing the background to establish potential pharmacological targets based on sst(2) pharmacology.

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Section: Electroretinographic Responses and Hypoxia Effectsmentioning

confidence: 99%

Section: Sst 2 Role In Retinal Functionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Protective role of somatostatin receptor 2 against retinal degeneration in response to hypoxia

Monte

Latina

Cupisti

et al. 2012

Naunyn-Schmiedeberg's Arch Pharmacol

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“…OPL thinning, reduced horizontal cell count) with a permanent deficit of retinal function (significantly attenuated scotopic and photopic ERGs) [1][2][3][4][5]. In comparison, postnatal hyperoxia exerts an even greater loss of retinal structure and function in the pigmented LE rat (greater vascular dropout, generalized deficit to retinal cytoarchitecture, more severely attenuated retinal function) [7].…”

Section: Managing Rop: Lessons From Oirmentioning

confidence: 99%

“…Previous studies of ours revealed that the structural (retinal histology) and functional (electroretinogram) deficits that resulted from the exposure of albino Sprague Dawley (SD) rats to a hyperoxic environment within the first postnatal days were permanent [1][2][3][4][5]. This contrasts with the damage to the retinal vasculature which can, as previously documented by others as well, overcome the hyperoxic challenge thereby achieving full coverage while still under oxygen throughout the first 2 weeks of life [1].…”

Section: Introductionmentioning

confidence: 99%

Postnatal hyperoxia and the developing rat retina: beyond the obvious vasculopathy

2009

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Although a great deal of emphasis has been placed on the vasculopathy that is associated with oxygen-induced retinopathy (OIR), our studies also revealed significant and irreversible structural (retinal histology) and functional (scotopic and photopic electroretinograms) impairments that were significantly more severe in pigmented Long-Evans rats compared to the more commonly used albino Sprague Dawley rats. In the following pages, we will highlight what we have learned about the retinal pathophysiological processes of OIR taking place in strains of both rats with the hope that this will trigger investigations into new therapeutic strategies to complement those geared at preventing the vasculopathy.

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The effect of oxygen and light on the structure and function of the neonatal rat retina

et al. 2008

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The neonatal rat is born with its eyes closed and an immature visual system, that some say is equivalent to that of a human fetus at 26 weeks of gestation. From birth, the visual system of the newborn rat will gradually mature, the first manifestation of that being the opening of the eye which usually take place at postnatal day 14. Complete maturation of the retina and visual pathways is normally reached at the end of the first month of life. The neonatal rat model thus represents a unique paradigm to study the normal and abnormal maturation of the primary visual pathways that normally occurs in utero in human subjects. Our laboratory has, over the past decade, developed two animal models of postnatally induced retinopathy, namely the Oxygen-Induced Retinopathy (OIR) that share several common features with the human Retinopathy of Prematurity (ROP) and the Light-Induced Retinopathy that is viewed by some as a valid model of some forms of Retinitis Pigmentosa (RP). The following pages review what is known of the pathophysiological processes taking place and suggest possible therapeutic avenues that could be explored in order to halt the degenerative process.

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Structural and Functional Consequences of Trolox C Treatment in the Rat Model of Postnatal Hyperoxia

Cited by 19 publications

References 27 publications

Protective role of somatostatin receptor 2 against retinal degeneration in response to hypoxia

Protective role of somatostatin receptor 2 against retinal degeneration in response to hypoxia

Postnatal hyperoxia and the developing rat retina: beyond the obvious vasculopathy

The effect of oxygen and light on the structure and function of the neonatal rat retina

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