Abstract
It is now generally recognized that stressful events play a critical role in the genesis of psychopathology. The neurobiological mechanisms that mediate the contribution of stressful events to the manifestation of psychiatric disorders may include changes in synaptic efficacy in different brain areas. Numerous studies in animals have begun to identify some of these areas through experiments manipulating stressful components. This review focuses on alterations of synaptic efficacy in the hippocampus, the lateral septum, and the medial prefrontal cortex that mimic the pathophysiology of depression and post-traumatic stress disorder.