Glucagon amacrine cells regulate ocular growth and refraction in chick

Recently, the immediate-early gene ZENK was identified as the first marker to change in response to the sign of defocus (Fischer et al., 1999). This marker was localized to glucagon amacrine cells, implicating them and the peptide glucagon as regulators of ocular growth. In this study I tested whether glucagon mediates control of ocular growth by using exogenous glucagon agonists to prevent myopia and antagonists to prevent recovery from myopia. Glucagon agonists prevented the excessive growth and negative refraction associated with form-deprivation myopia and induced the choroids of the treated eyes to thicken. Glucagon antagonists inhibited the growth restraint associated with plus-lens wear and prevented full recovery of refractive error from form-deprivation myopia. These observations suggest that glucagon amacrine cells and glucagon itself comprise a vision-dependent mechanism for growth-restraint in the chick eye. The inability of the antagonist to prevent growth-restraint during recovery from myopia suggests that additional pathways are involved in restoring emmetropia to previously deprived eyes.