The popular theory “Stress acceleration hypothesis” asserts that early life stress such as maternal separation speeds up the developmental process in the brain to result in adult-like learning processes, including conditioned fear extinction, which may cause some premature vulnerability to express fear early in life. However, the neural evidence supporting this idea has been scarce, with evidence largely limited to the amygdala. In addition, sex-specific impact of chronic stress on the hypothalamic-pituitary-adrenal (HPA) axis response following fear conditioning in juvenile and adolescent rats is poorly understood. We have exciting new data on sex-specific extinction of conditioned fear, neurogenesis, and the hypothalamic-pituitary-adrenal (HPA) axis that challenge the dogma on how early life stress changes the speed of brain development. New data on neurogenesis and HPA axis suggest that females’ resistance against stress effects on conditioned fear extinction early in life. We propose a new “Stress prolonged puberty hypothesis” that theorises early life stress accelerates amygdala development while delaying prefrontal cortex and hippocampal development to result in extinction-resistant fear expression. This new hypothesis brings together accumulating evidence in rodents and humans to provide an innovative framework to understand the role of early life stress in health and disease.
　　　　　　　　　　　　　　　　　　　(Co-organized by Department of Integrative Physiology)

▼Seminar poster