The matured eye of Xenopus laevis tadpoles produces factors that elicit a lens-forming response in embryonic ectoderm.

Previous studies have indicated that the outer cornea can undergo transdifferentiation to form a lens in the tadpole larva of Xenopus laevis following removal of the original lens. This transformation appears to require an interaction with the neural retina. In the present study, we carried out a series of experiments to determine if the matured tadpole eye can also elicit lens formation in embryonic ectoderm. Labeled embryonic ectoderm was removed from the presumptive lens-forming region, or from the belly region (ventral ectoderm), at various stages of development (stages 11-19, gastrula to neural tube stages) and implanted into the eye cavity (posterior chamber) of advanced stage 52-55 tadpoles. After 3 days, we examined the tadpoles and their implanted tissues for lens cell formation using lens-specific antibodies. Implanted presumptive lens ectoderm differentiated lens cells in a large number of cases. The percentage of cases forming lens cells and the extent of morphological differentiation increased with increasing age of the implanted tissue. Implanted ventral ectoderm also formed lens cells, although at a reduced frequency and with limited morphological differentiation. These results indicate that the environment of the matured tadpole eye cavity stimulates lens cell formation in both presumptive lens and nonlens ectoderm. The development of the implanted tissues was compared to that found in previous studies where these tissues were cultured as explants or transplanted to lens-forming regions during early development and subjected to various periods of embryonic lens induction. Together, these findings suggest that the process of embryonic lens formation is related to that involved in transdifferentiation of the tadpole cornea during "lens regeneration." However, the inductive effect of the matured tadpole eye is qualitatively different from that of the early period of embryonic lens induction and, while more intense, may be more closely related to that which takes place via the optic vesicle during the later phase of embryonic lens induction.

Responsiveness of intracardiac neurons to cholinergic stimulation in normal and thyroidectomized dogs.

Hypothyroidism alters the responsiveness of sympathetically innervated structures. The present work was done to determine if the responsiveness of the intrinsic cardiac nerves (ICN) to nicotine is also affected by thyroidectomy (THX). Mongrel dogs were anesthetized and an electrode catheter was advanced into the right atrium for recording His bundle activity (HB). A second cannula was placed into the carotid artery with its tip near the coronary ostia, so that the responses to the drugs injected would be confined to the heart. Changes in the A-H interval of the HB were recorded in response to both acetylcholine (ACH) 2-50 ug, and nicotine HCl (NIC) 5-100 ug, before and after beta blockade with metoprolol (1-4 mg). There were no important differences between the two groups in the responses of A-V nodal conduction to ACH over the dose range used. However, the THX animals showed an apparent increase in responsiveness to NIC; ie., ca. 5% decrease in A-H at 10 ug (control) compared to ca. 30% increase after THX. The apparent catecholamine-releasing effect of NIC was also enhanced in the THX animals. In addition, the responses to ACH and NIC were compared in animals both 'on' and 'off' cardiac bypass. The data suggest that hypothyroidism increases the effectiveness of nicotinic stimulation of intracardiac neurons.