Endogenous opiates in the chick retina and their role in form-deprivation myopia.

In this study, the possible role of the retinal enkephalin system in form-deprivation myopia (FDM) in the chick eye was investigated. Daily intravitreal injection of the nonspecific opiate antagonist naloxone blocked development of FDM in a dose-dependent manner, while injection of the opiate agonist morphine had no effect at any dose tested. The ED50 for naloxone (calculated maximum concentration in the vitreous) was found to be in the low picomolar range. The results using receptor-subtype-specific drugs were contradictory. Drugs specific for mu and delta receptors had no effect on FDM. The kappa-specific antagonist nor-binaltorphimine (nor-BNI) reduced FDM by about 50% at maximum daily retinal doses ranging between 4 x 10(-10) and 4 x 10(-7) M, while the kappa-specific agonist U50488 blocked FDM in a dose-dependent manner with an ED50 between 5 x 10(-8) and 5 x 10(-7) M. Met-enkephalin immunoreactivity (ME-IR) was localized immunocytochemically to a subset of amacrine cells (ENSLI cells) and their neurites in the inner plexiform layer (IPL). As reported previously, ENSLI cells from untreated chick retinas showed a cyclical pattern of immunoreactivity, with increased immunoreactivity in the light compared to the dark. Form-deprivation did not appear to change this pattern. Amounts of preproenkephalin mRNA from normal or form-deprived eyes were approximately the same under all conditions. Daily injection of naloxone, however, did increase ME-IR in the dark. These results suggest that naloxone may affect release of enkephalin from the ENSLI cells. The results as presented are inconclusive with regards to the role of the enkephalin system in FDM. While the kappa receptor may participate, there is no conclusive evidence here for a direct effect of opiate receptors. The effect of naloxone on form-deprived eyes may be due to its effect on release of peptides from the ENSLI cells.