Abstract
The ipsilateral retinothalamic projection in Xenopus laevis normally first appears at about stage 54, at a time when a number of other changes known to be dependent on a rise in circulating levels of thyroxine begin to occur. We have investigated the role of thyroxine in the development of the ipsilateral retinothalamic projection by studying retinal projections and patterns of retinal histogenesis in tadpoles whose ability to produce thyroxine was blocked by treatment with propylthiouracil (PTU), and in similar tadpoles in which thyroxine was restored by injection of small amounts of thyroxine into one eye. PTU-reared tadpoles continue to grow and to add neurons to the retina in a symmetric pattern like that of normal tadpoles at early developmental stages. The PTU-reared tadpoles remained by external criteria at stage 54. Like normal stage 54 tadpoles, the PTU-reared tadpoles either lacked an ipsilateral projection entirely or had an extremely sparse projection. Injection of thyroxine into one eye of PTU- reared tadpoles resulted in the production of substantial ipsilateral projections from the treated eyes as well as shifts to the asymmetric pattern of retinal cell addition which normally begins after stage 54. Such changes were much more prominent in hormone-treated than in untreated eyes, suggesting that they are caused by local action of thyroxine on the treated eyes. With low doses, thyroxine-induced effects on the development of the ipsilateral projection and on retinal histogenesis were restricted to the treated eye. These results suggest that the presence of thyroxine in one eye alone is sufficient to cause the development of the ipsilateral projection.
