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Kainic acid and formoguanamine effects on environmentally-induced eye lesions in chicks
1Department of Zoology, University of Alberta, Edmonton, Canada.
Abstract:
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.
Insights
Pharmacological blindness in chicks prevented myopia development but not glaucoma-related eye enlargement, suggesting vision drives myopia but not all glaucoma aspects.
Area of Science:
- Ophthalmology
- Neuroscience
- Developmental Biology
Background:
- Vision plays a crucial role in ocular development and the pathogenesis of certain eye conditions.
- Neurotoxins offer a method to selectively target visual pathways and study the impact of vision loss.
Purpose of the Study:
- To investigate the role of vision in the development of light-induced avian glaucoma (LIAG) and lid-suture myopia (LSM) using pharmacologically induced blindness in chicks.
- To differentiate between vision-dependent and independent mechanisms in the pathogenesis of LIAG and LSM.
Main Methods:
- Chicks were rendered pharmacologically blind using neurotoxins like formoguanamine, kainic acid, and quisqualic acid.
- Experimental models for light-induced avian glaucoma (LIAG) and lid-suture myopia (LSM) were employed.
- Ocular parameters including eye weight, globe enlargement, axial length, and anterior segment changes were measured.
Main Results:
- Formoguanamine-induced blindness prevented the development of lid-suture myopia (LSM).
- Pharmacological blindness did not prevent the anterior segment changes associated with light-induced avian glaucoma (LIAG).
- Kainic acid and quisqualic acid, retinal neurotoxins, failed to prevent globe enlargement in LIAG or LSM models, indicating these processes are not solely vision-dependent.
Conclusions:
- Globe enlargement in LIAG and axial lengthening in LSM appear to be vision-driven processes.
- Anterior segment changes in LIAG are likely regulated by mechanisms independent of vision.
- Retinal neurotoxins like kainic acid and quisqualic acid do not fully prevent the ocular changes associated with LIAG and LSM.
