Endogenous opiates in the chick retina and their role in form-deprivation myopia

Seltner, Ruth L. Pickett; Rohrer, Bäerbel; Grant, Vincent; Stell, William K.

doi:10.1017/s0952523800011548

Cited by 27 publications

(13 citation statements)

References 44 publications

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“…However, retinal proenkephalin levels were unaffected by FDM, leaving the authors to interpret their results as inconclusive [177]. While this and the other peptide studies cited earlier offer insight into the signaling mechanisms underlying the development of myopia – specifically, they point to involvement of the inner retina in signal processing – there have been no recent follow-up studies of those covered in the aforementioned discussion.…”

Section: Drug Studies Involving Animal Models For Myopiamentioning

confidence: 99%

Pharmaceutical intervention for myopia control

Ganesan

Wildsoet

2010

Expert Review of Ophthalmology

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Myopia is the result of a mismatch between the optical power and the length of the eye, with the latter being too long. Driving the research in this field is the need to develop myopia treatments that can limit axial elongation. When axial elongation is excessive, as in high myopia, there is an increased risk of visual impairment and blindness due to ensuing pathologies such as retinal detachments. This article covers both clinical studies involving myopic children, and studies involving animal models for myopia. Atropine, a nonselective muscarinic antagonist, has been studied most extensively in both contexts. Because it remains the only drug used in a clinical setting, it is a major focus of the first part of this article, which also covers the many shortcomings of topical ophthalmic atropine. The second part of this article focuses on in vitro and animal-based drug studies, which encompass a range of drug targets including the retina, retinal pigment epithelium and sclera. While the latter studies have contributed to a better understanding of how eye growth is regulated, no new antimyopia drug treatments have reached the clinical setting. Less conservative approaches in research, and in particular, the exploration of new bioengineering approaches for drug delivery, are needed to advance this field. Keywordsanimal models; atropine; clinical trials; dopamine; eye growth; growth factors; myopia Myopia describes the refractive error in which light entering the eye from distant objects is focused in front of the retina, leading to blurred vision. The condition is most commonly the result of excessive elongation of the posterior vitreous chamber of the eye, increasing the risk of retinal detachment and some degenerative retinal conditions, and rendering high myopia a major cause of visual impairment and blindness [1][2][3][4][5][6]. Myopia has become a major public health concern owing to rapid rises in the prevalence of myopia, first noted in East Asian populations. For example, as of the year 2000, the prevalence of myopia had reached 84% for Taiwanese adolescents between 16 and 18 years of age. Of the 18-yearolds, 21% were highly myopic, putting them at high risk for pathologic conditions in the future [7]. Similar trends are evident in recently published myopia prevalence figures for the USA, although they are not as high as East Asian figures [8][9][10][11].The management of myopia has been mostly directed at correcting the mismatch between the eye's optical power and its length using either optical means, such as single-vision spectacles and contact lenses, or refractive surgeries, such as photorefractive keratectomy (PRK) and laser-assisted in situ keratomileusis (LASIK), which both involve reshaping and thus modifying the optical power of the cornea. While these options restore sharp distance vision in myopes, they do nothing to control myopia progression. On the other hand, the © 2010 Expert Reviews Ltd † Author for correspondence: prema@berkeley.edu. NIH Public Access Author ManuscriptExpert Rev O...

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Section: Drug Studies Involving Animal Models For Myopiamentioning

confidence: 99%

Pharmaceutical intervention for myopia control

Ganesan

Wildsoet

2010

Expert Review of Ophthalmology

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“…Eye growth seems to be controlled locally, perhaps in the retina. Although no consensus has been reached on the exact site of regulation, many studies have implied the existence of a local regulatory circuit in the neurons of the proximal retina, [27][28][29][30][31][32][33][34][35][36] where Shh and its downstream mediators are located. A change in environmental lighting can change Shh mRNA expression in mice retinas.…”

Section: Altered Expression Of Shh-signaling Factors In Experimental mentioning

confidence: 99%

Sonic Hedgehog Expression and Its Role in Form-Deprivation Myopia in Mice

Qian

Chu

et al. 2009

Current Eye Research

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“…Pharmacological antagonists to opiate, VIP, and muscarinic acetylcholine receptors suppress FDM (for review, see Wallman, 1993;Seltner et al, 1995;Seltner et al, 1997). The conventional interpretation of these findings would be that the corresponding endogenous ligands (ENK, VIP, and ACh) released from retinal cells are responsible for FDM.…”

Section: Destruction Of Amacrine Cells Involved In Ocular Growth Regumentioning

confidence: 99%

Immunocytochemical characterization of quisqualic acid- and N-methyl-D-aspartate-induced excitotoxicity in the retina of chicks

et al. 1998

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A single, large dose of N-methyl-D-aspartate (NMDA) or quisqualic acid (QA) injected into the chick eye has been shown previously to destroy many retinal amacrine cells and to induce excessive ocular growth accompanied by myopia. The purpose of this study was to identify distinct populations of retinal cells, particularly those believed to be involved in regulating ocular growth, that are sensitive to NMDA or QA. Two pmol of NMDA or 0.2 micromol of QA were injected unilaterally into eyes of 7-day-old chicks, and retinas were prepared for observation 1, 3, or 7 days later. Retinal neurons were identified by using immunocytochemistry, and cells containing fragmented DNA were identified by 3'-nick-end labelling in frozen sections. NMDA and QA destroyed many amacrine cells, including those immunoreactive for vasoactive intestinal polypeptide, Met-enkephalin, and choline acetyltransferase, but they had little effect upon tyrosine hydroxylase-immunoreactive cells. Other cells affected by both QA and NMDA included those immunoreactive for glutamic acid decarboxylase, gamma-aminobutyric acid, parvalbumin, serotonin, and aminohydroxy methylisoxazole propionic acid (AMPA) receptor subunits GluR1 and GluR2/3. Cells largely unaffected by QA or NMDA included bipolar cells immunoreactive for protein kinase C (alpha and beta isoforms) and amacrine cells immunoreactive for glucagon. DNA fragmentation was detected maximally in many amacrine cells and in some bipolar cells 1 day after exposure to QA or NMDA. We propose that excitotoxicity caused by QA and NMDA induces apoptosis in specific populations of amacrine cells and that these actions are responsible for the ocular growth-specific effects of QA and NMDA reported elsewhere.

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Endogenous opiates in the chick retina and their role in form-deprivation myopia

Cited by 27 publications

References 44 publications

Pharmaceutical intervention for myopia control

Pharmaceutical intervention for myopia control

Sonic Hedgehog Expression and Its Role in Form-Deprivation Myopia in Mice

Immunocytochemical characterization of quisqualic acid- and N-methyl-D-aspartate-induced excitotoxicity in the retina of chicks

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