The research proposes a continuation of studies on experimental epilepsy and the investigation of another neural model in order to arrive at further definitions of synaptic mechanisms involved in plastic changes in the nervous system. Previous work has shown that undercut, epileptic cerebral cortex shows electrical signs of supersensitivity, loss of dendritic spines, loss of axon collateral branches and lengths, a decrease in total AChE, a decrease in synaptic membrane specific AChE, and increased binding in the synaptic membranes for tubocurarine, an AChE competitor. The most important observation is that all of these changes can be prevented by daily electrical stimulation of the undercut cortex during the period when the changes normally would be developing. The proposed research involves three questions: 1) "Are there ultrastructural changes in denervated cortical neurons subjected to long-term stimulation?" 2) "Can expected degenerative synaptic changes in partially deafferentated cortical neurons be prevented by continued or increased use of remaining afferent structures?" and 3) "Do synaptic contact areas (dendritic spines) and other elements in intact cerebral cortex reflect increased activity (facilitation) in a system involving them? Experiments for question 1) will be on cats with undercut cortices. Some of these will have implanted electrodes or long-term stimulation. Study of question 2) will be on cats with eye enucleation and some of these will have electrodes in a lateral geniculate body for long-term stimulation. Question 3) will involve study of a pathway linking the two hemispheres in intact cats. The research is concerned not only with continued work on basic mechanisms of epilepsy but also with the theoretical problems of "use" and "disuse" in the nervous system.