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1 From the Department of Ophthalmology, Scheie Eye Institute; and 2 Department of Neuroscience, University of Pennsylvania School of Medicine, Philadelphia.
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 
7 and 8
subunits, which are highly expressed in chick retina. It showed a less
dramatic but still significant inhibitory effect on myopia. The effects
of dihydro-ß-erythroidine, a competitive antagonist relatively
selective for nicotinic receptors with 3 or 4 subunits and
particularly for 3ß2-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 RPE.
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