Effects of intravitreally and intraperitonally injected atropine on two types of experimental myopia in chicken

Diether, Sigrid; Schaeffel, Frank; Lambrou, George N.; Fritsch, Christine; Trendelenburg, Anne‐Ulrike

doi:10.1016/j.exer.2006.09.019

Cited by 56 publications

(52 citation statements)

References 23 publications

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“…Atropine, a non-selective muscarinic receptor antagonist, is currently the most potent agent used to prevent myopia in animal models and children (9). It has been reported that regular topical administration of 0.025% atropine eye drops can prevent myopia onset and myopic shift in premyopic school children for a 1-year period (10).…”

Section: Introductionmentioning

confidence: 99%

E-cadherin and 5-HT alterations in the heart of rats having undergone atropine-induced toxicity

Huang

Liu

2011

Mol Med Report

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Abstract. Atropine-induced heart damage is associated with changes in the expression of various enzymes and proteins. The purpose of this study was to investigate atropine-induced alterations in cardiac E-cadherin and 5-hydroxytryptamine (5-HT) after atropine administration. Male Wistar rats were randomly divided into two groups: a control group and an atropine group. The atropine group intraperitoneally received atropine at a single dose of 15 mg/kg for 7 days; the controls received the same amount of saline via the same route. On Day 8, the rats were anesthetized, and a thoracotomy was performed in all animals. Immunohistochemical analysis was performed to evaluate protein expression of E-cadherin and 5-HT. Sections were analyzed by digital image analysis. Cardiac protein expression of E-cadherin and 5-HT was altered after atropine-induced toxicity in the rat. The expression levels of E-cadherin and 5-HT were significantly decreased after atropine treatment, supported by IOD analysis, when compared with the control (P<0.05). The current findings indicate that such changes would be reflected in abnormal cardiac function, and these proteins may be useful for revealing the mechanisms underlying atropine-induced toxicity and may also provide various clues for further research.

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Section: Introductionmentioning

confidence: 99%

E-cadherin and 5-HT alterations in the heart of rats having undergone atropine-induced toxicity

Huang

Liu

2011

Mol Med Report

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“…Further, several non-selective (atropine [Diether et al, 2007]; atropine and oxyphenonium [Nickla et al, 2013a]) and partly selective (pirenzepine [Nickla et al, 2013a], M4 [Arumugam and McBrien, 2012]) muscarinic antagonists have also been found to prevent the axial eye elongation in animals treated with hyperopic defocus or to prevent the choroidal thinning that is normally associated with form-deprivation myopia (McBrien et al, 2011). Collectively, these observations suggest that choroidal thickening could be a part of a signalling cascade that mediates ocular growth inhibition (Nickla and Wallman, 2010a;Nickla et al, 2013a).…”

Section: Introductionmentioning

confidence: 87%

“…In animal studies, choroidal thickness and ocular growth changes have been shown to be influenced by non-selective, partially selective or highly selective muscarinic antagonists (i.e., atropine, pirenzepine, himbaicine, MT3, MT7) implicating muscarinic involvement in eye growth and myopia control (Arumugam and McBrien, 2012;Luft et al, 2003;Diether et al, 2007). Results from human clinical trials also indirectly support this hypothesis, with outcomes demonstrating that daily administration of the nonselective muscarinic antagonist 1% atropine, reduced the progression of myopia by about 60% during the second year of treatment, and concentrations as low as 0.01% atropine still reduced eye growth by 50% (Chua et al, 2006;Chia et al, 2012).…”

Section: Discussionmentioning

confidence: 99%

“…Further evidence for M4 receptor involvement in myopia prevention also came from McBrien et al (2011), who demonstrated both inhibition of form deprivation myopia and choroidal thinning after MT3 administration, but it was only partially effective at preventing the compensation to negative lenses in chicks (Diether et al, 2007).…”

Section: The Autonomic Innervation Of the Choroidmentioning

confidence: 99%

“…Although the identification of the site of action for muscarinic antagonists, has proven elusive, emerging data mostly from animal studies suggest that parasympathetic innervation in the choroid promotes compensatory choroidal responses that play an important part in the refractive error development cascade (Schmid and Wildsoet, 2004;Diether et al, 2007;Nickla and Wallman, 2010a;Nickla and Schrödl, 2012;Nickla et al, 2013a). The choroid contains a rich autonomic vasoactive nerve supply, which entails the activation of sympathetic adrenergic and parasympathetic muscarinic receptors.…”

Section: Introductionmentioning

confidence: 99%

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The Influence of the Autonomic Nervous System on the Human Choroid

Sander¹

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v AbstractThe impact of myopia is greater than just its optical consequences and in severe cases it can lead to a loss of vision. It is a highly prevalent eye disorder, with about one third of the population worldwide affected by this refractive error. Despite extensive research, the pathogenesis of myopia is still only partially understood. An improved knowledge of mechanisms underlying myopia is critical to developing new therapies to prevent myopia or to slow its progression.Although there is no fully effective and satisfactory myopia control treatment available, growing evidence has suggested that the choroid has a passive or active role in the regulation of eye growth and refractive error development. Numerous human and animal studies have shown that the retina can be moved forward or backward towards the image plane through changes in choroidal thickness, and these changes are likely to be associated in the longer term with eye growth and the development of refractive errors. As the choroid receives a rich innervation from the autonomic nervous system, many previous animal studies have utilized pharmacological agents and neurotoxins to elucidate the possible role of muscarinic signaling in the regulation of choroidal thickness, but only a few studies have investigated this issue in humans. An improved understanding of the mechanisms that control choroidal thickness may be important in developing new therapies for combating the development and progression of myopia.The research described in the thesis aimed to investigate the role of the autonomic nervous system in the control of choroidal thickness, axial length and the morphology In a series of experiments, we have confirmed that in humans under normal visual conditions, the parasympathetic nervous system is involved in the short-term regulation of subfoveal and parafoveal choroidal thickness, axial length and the morphology of the anterior sclera. The muscarinic blocker homatropine caused a significant subfoveal and parafoveal choroidal thickening, shortening of axial length, an enlargement of Schlemm's canal area and an increase in thickness of the conjunctival/episcleral complex. On the other hand, no notable changes in ocular parameters, except a decrease in the thickness of the conjunctival/episcleral tissues were found after instillation of the sympathomimetic drug phenylephrine.In an attempt to further improve our understanding of the myopigenic mechanisms influencing the thickness of the choroid in humans, we investigated the short-term influence of mixed interventions (positive and negative lens-imposed defocus / 2% homatropine) on choroidal thickness and axial length in emmetropic and myopic subjects. Homatropine prevented choroidal thinning in response to hyperopic defocus.This finding is consistent with the anti-myopia effects of muscarinic blockers and supports the potential importance of hyperopic defocus in the development of human myopia. By contrast, co-administration of homatropine with myopic defocus did not enhance the thicken...

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Muscarinic Receptor Agonists and Antagonists: Effects on Ocular Function

Mitchelson

2011

Handbook of Experimental Pharmacology

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Muscarinic agonists act mainly via muscarinic M₃ cholinoceptors to cause contraction of the iris sphincter, ciliary muscle and trabecular meshwork as well as increase outflow facility of aqueous humour. In the iris dilator, the effect of muscarinic agonists is species dependent but is predominantly relaxation via muscarinic M₃ receptors. In the conjunctiva, muscarinic agonists stimulate goblet cell secretion which contributes to the protective tear film. Muscarinic M₂ and M₃ receptors appear mainly involved. In the lens muscarinic agonists act via muscarinic M₁ receptors to produce depolarization and increase [Ca(2+)](i). All five subtypes of muscarinic receptor are present in the retina. In the developing retina, acetylcholine appears to limit purinergic stimulation of retinal development and decrease cell proliferation. In the adult retina acetylcholine and other muscarinic agonists may have complex effects, for example, enhancing light-evoked neuronal firing in transient ON retinal ganglion cells and inhibiting firing in OFF retinal ganglion cells. In the lacrimal gland, muscarinic agonists activate M₃ receptors on secretory globular acinar cells to stimulate tear secretion and also cause contraction of myoepithelial cells. In Sjögren's syndrome, antibodies to the muscarinic M₃ receptor disrupt normal gland function leading to xerophthalmia although the mechanism of action of the antibody is still not clear. Atropine and pirenzepine are useful in limiting the development of myopia in children probably by an action on muscarinic receptors in the sclera, although many other muscarinic receptor antagonists are not effective.

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Effects of intravitreally and intraperitonally injected atropine on two types of experimental myopia in chicken

Cited by 56 publications

References 23 publications

E-cadherin and 5-HT alterations in the heart of rats having undergone atropine-induced toxicity

E-cadherin and 5-HT alterations in the heart of rats having undergone atropine-induced toxicity

The Influence of the Autonomic Nervous System on the Human Choroid

Muscarinic Receptor Agonists and Antagonists: Effects on Ocular Function

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