Control of the development of the ipsilateral retinothalamic projection in Xenopus laevis by thyroxine: results and speculation.

The ipsilateral retinothalamic projection of the frog Xenopus laevis is formed by the axons of a subset of retinal ganglion cells which are found throughout peripheral and non-nasodorsal retina. Unlike the crossed retinotectal and retinothalamic projections, which begin to form during early embryonic stages, the ipsilateral projection does not begin to develop until late in tadpole life, at stages when thyroxine first becomes detectable in the circulation. Blocking the production of thyroid hormone in tadpoles prevents the development of the ipsilateral projection, in a reversible manner. Intraocular injection of thyroxine can "rescue" the development of the projection in tadpoles which otherwise remain premetamorphic. In addition, the projection from one eye of a metamorphically-blocked tadpole can be induced to form by an intraocular injection of thyroxine at a dose which has no detectable effect on retinal development in the other, untreated eye. These results indicate that the development of the ipsilateral retinothalamic projection is dependent upon thyroxine, and strongly suggest that the hormone acts at the level of the eye, rather than at the optic chiasm or thalamic target, to bring about the development of a new pathway. A number of ways in which thyroxine might act in the system are discussed.