oxadiazoles and Blindness

Several neurotoxins are known which destroy some specific retinal component or other link in the visual pathway. We have employed such reagents to induce blindness in chicks, in order to explore the role of vision in the development of light-induced avian glaucoma (LIAG) and/or lid-suture myopia (LSM). Chicks made pharmacologically blind with formoguanamine failed to develop LSM. Under LIAG conditions, increased eye weight and global enlargement did not occur, but the characteristic anterior segment changes were seen. Thus LIAG globe enlargement, and LSM axial lengthening, appear to be vision-driven, but anterior segment changes are probably separately controlled. The retinal neurotoxin kainic acid rendered chicks behaviorally blind in the eye into which it was injected intravitrially, but this failed to prevent LIAG changes in either anterior segment or growth of the globe. Chicks reared under LSM conditions, and treated with kainic acid were not different from untreated controls, in that they developed globe enlargement in spite of their pharmacologically-induced blindness. Preliminary trials with quisqualic acid, another retinal neurotoxin, indicate that this agent, like kainic acid, cannot prevent LIAG eye enlargement. Several quis-treated eyes developed phthisis bulbi however, and thus could not be included among those assessed for eye weight and dimensional measurements.

Topics: Animals; Blindness; Chickens; Cornea; Disease Models, Animal; Glaucoma; Kainic Acid; Light; Myopia; Organ Size; Oxadiazoles; Quisqualic Acid; Retina; Triazines; Vision, Ocular