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Richard A. Stone, Reiko Sugimoto, Amarjeet S. Gill, Ji Liu, Cheryl Capehart, Jon M. Lindstrom; Effects of Nicotinic Antagonists on Ocular Growth and Experimental Myopia. Invest. Ophthalmol. Vis. Sci. 2001;42(3):557-565.
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purpose. To learn whether nicotinic cholinergic receptors modulate postnatal eye
growth and influence the course of form-deprivation myopia.
methods. One-week-old White Leghorn chicks wore a unilateral goggle to induce
form-deprivation myopia. Other chicks were never goggled. Nicotinic
antagonist drugs were administered by intravitreal injection, usually
daily or every other day to the goggled eye or to one eye of
never-goggled chicks. After 1 week, the eyes were studied by
refractometry, A-scan ultrasonography, and caliper measurements.
results. The relatively non–subtype-specific channel-blocking nicotinic
antagonists chlorisondamine and mecamylamine each inhibited the
development of form-deprivation myopia but with complex multiphasic
dose responses. Chlorisondamine was the most effective. Mecamylamine,
at the lowest tested doses, tended to stimulate the growth response and
myopic refractive shift of goggle wearing. Methyllycaconitine
competitively inhibits nicotinic receptors containing the α7 and α8
subunits, which are highly expressed in chick retina. It showed a less
dramatic but still significant inhibitory effect on myopia. The effects
of dihydro-β-erythroidine, a competitive antagonist relatively
selective for nicotinic receptors with α3 or α4 subunits and
particularly for α3β2-containing receptors, were the weakest and
inhibited primarily axial elongation. Chlorisondamine but not
mecamylamine also affected nongoggled eyes, inhibiting growth and
shifting refraction toward hyperopia, but chlorisondamine also induced
degenerative changes to the retinal pigment epithelium (RPE).
conclusions. Nicotinic receptors are involved in eye growth control. Nicotinic
antagonists affect the development of form-deprivation myopia and
perhaps the growth of nongoggled eyes. The differences in drug activity
and multiphasic dose–response curves may reflect the complexity of
nicotinic receptor subtypes associated with the eye and/or
pharmacokinetic differences between the individual drugs. Although
another tissue(s) cannot be completely excluded by these data, the site
of action of these agents may be neural retina or
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