Visual experience is one of the factors that influences the formation of orderly connections in the developing tectum of the frog, Xenopus laevis. Input from the ipsilateral eye is relayed to the tectum via the nucleus isthmi (NI), and this ipsilateral map normally is in register with the map which is relayed from the contralateral eye via the optic nerve. The matching-up of the two maps is dependent on visual input during development. Abnormal visual input, resulting from experimental rotation of one eye, can induce isthmotectal axons to terminate in different sites than normal. These processes take place during a critical period of late tadpole-early postmetamorphic life, and plasticity normally is lost thereafter. NMDA receptors play an important role in plasticity. Blocking those receptors during the critical period blocks plasticity, and a three-month application of NMDA after the critical period fully restores plasticity. The following experiments are designed to investigate further the role of NMDA receptors by answering the following questions. 1. What doses of NMDA are effective in re-establishing plasticity in adults, and do those doses alter tectal activity? 2. Must NMDA be present for a full three months to restore plasticity? 3. What is the morphology of isthmotectal axons in NMDA-treated tecta? 4. Does the number of NMDA receptors normally change during development? 5. Can NMDA induce plasticity de novo in Rana pipiens, a species which normally shows no reorganization after eye rotation? Dark-rearing prolongs the critical period and affords another tool for assessing mechanisms of plasticity. Axon branching patterns and NMDA receptor numbers in dark-reared Xenopus will be studied. A deeper understanding of how convergent binocular input affects topography requires identification of the tectal cells which receive those inputs. Combined anterograde filling of isthmotectal axons and immunocytochemical labeling of tectal cells will serve to identify targets of isthmotectal axons.