STIMULATION OF DOPAMINERGIC AMACRINE CELLS BY STROBOSCOPIC ILLUMINATION OR FIBROBLAST GROWTH-FACTOR (BFGF, FGF-2) INJECTIONS - POSSIBLE ROLES IN PREVENTION OF FORM-DEPRIVATION MYOPIA IN THE CHICK

Form-deprivation myopia (FDM) in the chick is a popular model for stud ying the postnatal regulation of ocular growth. Using this model, we h ave shown previously that dopamine and FGF-2 can counteract the effect s of form-deprivation, thereby producing emmetropia. In the present st udy, we tested the hypothesis that the emmetropizing effects of flicke ring light and intraocular injections of FGF-2 in the chick are mediat ed by the activity of dopaminergic retinal amacrine cells. We have ass essed the rate of dopamine synthesis in the retina by measuring the ac cumulation of 3,4-dihydroxyphenylalanine (DOPA). We found that form-de privation reduces the rate of dopamine synthesis in the light-adapted retina, and that the normal rate of dopamine synthesis in the light ca n be restored by stroboscopic illumination at frequencies around 10 Hz . By labeling cells immunocytochemically we have shown that the synthe sis of c-fos, a putative transcriptional regulator of the tyrosine hyd roxylase gene, is induced in dopaminergic amacrine cells by stroboscop ic illumination at around 10 Hz. These observations are consistent wit h a critical role for dopaminergic amacrine cells in the regulation of ocular growth by intermittent illumination. We have found also that i ntraocular injections of FGF-2 cause emmetropization without altering levels of expression of c-fos, amounts of tyrosine hydroxylase, or rat es of dopamine synthesis with respect to vehicle-injected controls. We conclude that FGF acts either in parallel to or downstream from the d opaminergic amacrine cells, rather than through them. We observed that intravitreal injection per se induces high levels of c-fos expression in both form-deprived and non-deprived retinas, and causes partial em metropization in form-deprived eyes, while inhibiting dopamine synthes is in non-deprived retinas. It is likely, therefore, that injection st imulates the production and/or release of unknown factors whose divers e effects on ocular growth and dopamine metabolism are mediated by com plex pathways. Taken together, our results are consistent with the vie w that the retinal circuitry that controls postnatal ocular growth in the chick involves multiple messengers and pathways.