Effects of atropine on refractive development, dopamine release, and slow retinal potentials in the chick

Atropine has previously been found to suppress visually induced myopia both in animals and humans. The mechanism of its action is unclear. We have stu died its retinal effects in an in vitro preparation, using the retina-pigme nt epithelium-choroid complex of the chick eye. In vivo, deprivation myopia was induced by translucent goggles. Atropine solution was injected into th e vitreous at two-day intervals. Dopamine release from the retina following atropine injection in vivo and from the in vitro retina preparation was qu antified by HPLC-EC. In vitro preparations of the isolated chick retina-pig ment epithelium-choroid were superfused with atropine. Light-induced potent ials (local ERG), slow standing potentials fi om the retinal pigment epithe lium/neural retina, and extracellular potassium concentrations were recorde d. In line with previous findings, intravitreal injections of atropine (25 mu g, 250 mu g) reduced deprivation myopia in a dose-dependent manner. Atro pine increased the release of the neurotransmitter dopamine into the superf usate in vitro at 100-500 mu M and into the vitreous in vivo at 250 mu g. B efore an increase was measured in the vitreous, the retinal dopamine conten t was elevated. In concentrations equivalent to the intravitreal concentrat ion to suppress myopia in vivo (200-800 mu M), atropine induced spreading d epression (SD) in the in vitro preparation. In contrast, muscarinic agonist s, acetylcholine and pilocarpine, did not induce SD. Atropine reduced the E RG b- and d-wave, led to damped oscillations of RPE potentials, and reverse d the ERG c-wave. Atropine suppressed myopia only at doses at which severe nonspecific side effects were observed in the retina. Atropine seems to int rude massively into the vital functions of the retina as indicated by the o ccurrence of SD. We conclude that atropine, by inducing SD, boosts neurotra nsmitter release from cellular stores, which may cancel out a presumed reti nal signal that controls eye growth and through this, myopia.