The quantity of rhodopsin in human eyes

Fulton, Anne B.; Dodge, Janice; Schremser, Jeri-Lynn; Armstrong, A. Francis; Lanier, Fred; Dawson, William W.; Williams, Theodore P.

doi:10.3109/02713689009003477

Cited by 32 publications

(51 citation statements)

References 7 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The caliber of the retinal arterioles adjusts to perturbations in blood oxygen levels ("autoregulation"). Logistic growth curve showing human rhodopsin content [40] as a function of age. The red arrow indicates the age of ROP onset in preterm infants [41].…”

Section: Discussionmentioning

confidence: 99%

Retinal degenerative and hypoxic ischemic disease

et al. 2008

Self Cite

View full text Add to dashboard Cite

A broad spectrum of retinal diseases affects both the retinal vasculature and the neural retina, including photoreceptor and postreceptor layers. The accepted clinical hallmarks of acute retinopathy of prematurity (ROP) are dilation and tortuosity of the retinal vasculature. Additionally, significant early and persistent effects on photoreceptor and postreceptor neural structures and function are demonstrated in ROP. In this paper, we focus on the results of longitudinal studies of electroretinographic (ERG) and vascular features in rats with induced retinopathies that model the gamut of human ROP, mild to severe. Two potential targets for pharmaceutical interventions emerge from the observations. The first target is immature photoreceptors because the status of the photoreceptors at an early age predicts later vascular outcome; this approach is appealing as it holds promise to prevent ROP. The second target is the interplay of the neural and vascular retinal networks, which develop cooperatively. Beneficial pharmaceutical interventions may be measured in improved visual outcome as well as lessening of the vascular abnormalities.As a system, the mammalian retina is vulnerable to diseases that affect the exquisitely balanced interplay of the neural retina and the vasculature that nourishes it. Visual loss occurs when this balance is disturbed. On the one hand, diseases such as photoreceptor degenerations that primarily affect the neural retina also affect the retinal vasculature. On the other hand, diseases that are clinically characterized by abnormality in the choroidal or retinal vasculature, such as age related macular degeneration, diabetic retinopathy, and retinopathy of prematurity (ROP), also affect the retinal neurons. Thus, all such diseases fall within the broad group of hypoxic ischemic disorders of neural tissue. Photoreceptors, specialized cells that have the highest oxygen requirements of any cell in the body [1], are likely important in all hypoxic ischemic diseases of the retina. Translation from animal models to patientsThe photoreceptors are nestled closely to the choroidal vasculature (figure 1). Highly organized postreceptor retinal neurons form layers that are supplied by the retinal vessels. Although the choroid is the principal supply to the photoreceptors, degeneration of the photoreceptors is, nonetheless, associated with attenuation of the retinal arterioles [2]. Because the photoreceptor layer is such an extraordinary oxygen sink, it is presumed that, as photoreceptors degenerate, their metabolic demands wane and the retinal vasculature becomes attenuated consequent to the neural retina's chronic lower requirement for oxygen [2]. NIH-PA Author ManuscriptA tight link between the photoreceptors and the retinal vascular network is evident in the developing retina. Postreceptor cells differentiate before the photoreceptors, which are the last retinal cells to mature. As the formation of rod outer segments advances in a posterior to peripheral gradient, so too does vascular coverag...

show abstract

Section: Discussionmentioning

confidence: 99%

Retinal degenerative and hypoxic ischemic disease

et al. 2008

Self Cite

View full text Add to dashboard Cite

show abstract

“…These are two important issues which need to be noted in terms of retinal architecture and retinal metabolism: (1) During the last 12 weeks of a normal pregnancy, the retina develops rapidly [25][26][27]. Therefore, there are significant differences between retinal properties in premature infants with different gestation ages.…”

Section: The Human Retina Is Immature During Rop Developmentmentioning

confidence: 99%

Oxygen supply and consumption in the retina: implications for studies of retinopathy of prematurity

Cringle

2009

Doc Ophthalmol

View full text Add to dashboard Cite

A disrupted oxygen environment in the retina of severely premature neonates is thought to be a key factor in the development of retinopathy of prematurity (ROP). This review describes our understanding of intraretinal oxygen distribution and consumption in a range of animal models, including species with naturally avascular retinas and models of induced occlusion of the retinal vasculature. The influence of graded systemic hyperoxia on retinal oxygenation is also discussed along with modulation of retinal oxygen metabolism. The differences in retinal oxygenation between developing and mature retinas are also described. Comparisons are made with studies in the monkey retina in order to assess possible similarities in behaviour between rat and human retinas. Pathogenesis mechanism and possible intervention strategies during the diseased processes in ROP are proposed based on our current knowledge.

show abstract

“…The reduction in photoreceptor function (PIII/a-wave amplitude) could be explained by a reduction in photoreceptor numbers, outer segment length, or the number of cGMP gated channels expressed within photoreceptor outer segments. 25 Previous studies have reported a reduction in outer segment length in the rat 67 and mouse 10 models of OIR, with no change in the number of photoreceptor nuclei. 11 Until recently, it was not clear why photoreceptors were affected in OIR, given that the disease was generally believed to specifically affect the intraretinal blood vessels, while the choroidal vasculature, which supplies the photoreceptors, 68,69 was largely believed to be intact.…”

Section: Rats With Oir Have Deficits In Both Rod and Cone Pathway Funmentioning

confidence: 99%

The Vasoneuronal Effects of AT₁Receptor Blockade in a Rat Model of Retinopathy of Prematurity

Hatzopoulos

Vessey

Wilkinson-Berka

et al. 2014

Invest. Ophthalmol. Vis. Sci.

View full text Add to dashboard Cite

PURPOSE. Retinal angiogenesis, neural dysfunction, and microglial activation occur in both humans with retinopathy of prematurity and in animal models of the disease. The aim of this study was to assess whether blockade of the renin-angiotensin system ameliorated these effects in rats with oxygen induced retinopathy (OIR).METHODS. Sprague-Dawley rats were treated with 80% oxygen from birth to postnatal day (P)11 and were then placed in normal air until experimentation at P18, while control animals remained in normal air. Control and OIR rats were treated with the angiotensin II type 1 receptor (AT 1 receptor) antagonist, valsartan (4, 10, or 40 mg/kg daily, intraperitoneally). Retinal function was assessed using the twin-flash electroretinogram and immunocytochemistry was used to evaluate vascular change and microglial activation.RESULTS. Oxygen-induced retinopathy was associated with growth of blood vessels into the vitreous in the peripheral retina, increased microglial number, and activation and a reduction in both rod and cone pathway function. Although treatment with valsartan reduced growth of vessels into the vitreous, it also reduced the formation of the deep vascular plexus. Valsartan treatment reduced microglial number and activation; however, it did not ameliorate neural dysfunction. At the highest dose examined, valsartan treatment reduced photoreceptor and inner retinal function in both the control and OIR animals. CONCLUSIONS.Valsartan was effective in reducing physiological and pathological angiogenesis and the microglial inflammatory response, indicating a role for the AT 1 receptor in these processes, but it did not prevent retinal dysfunction. More work is needed to better understand the mechanisms underlying neuronal dysfunction in oxygen-induced retinopathy.

show abstract

The quantity of rhodopsin in human eyes

Cited by 32 publications

References 7 publications

Retinal degenerative and hypoxic ischemic disease

Retinal degenerative and hypoxic ischemic disease

Oxygen supply and consumption in the retina: implications for studies of retinopathy of prematurity

The Vasoneuronal Effects of AT₁Receptor Blockade in a Rat Model of Retinopathy of Prematurity

Contact Info

Product

Resources

About

The quantity of rhodopsin in human eyes

Cited by 32 publications

References 7 publications

Retinal degenerative and hypoxic ischemic disease

Retinal degenerative and hypoxic ischemic disease

Oxygen supply and consumption in the retina: implications for studies of retinopathy of prematurity

The Vasoneuronal Effects of AT1Receptor Blockade in a Rat Model of Retinopathy of Prematurity

Contact Info

Product

Resources

About

The Vasoneuronal Effects of AT₁Receptor Blockade in a Rat Model of Retinopathy of Prematurity