What Is Early Life Stress?

Stress, the disruption of the homeostatic balance by internal or external influences, is inherent, inevitable and exists in every stages of life, starting as early as the fetal stage till one’s death. In particular, early life stress (ELS) has come to light in recent years as it is becoming more prevalent and epidemiological studies have shown that ELS increases one’s vulnerability to subsequent stressors, leading to a multitude of stress-related neuropsychiatric disorders such as depression and post-traumatic stress disorder (PTSD) in adulthood. This is not surprising as the exposure to ELS corresponds to the maturation period of several brain structures, including amygdala and hippocampus. Consequently, this interference with post-natal neuronal
development can potentially induce lasting structural and behavioral alterations, which in turns increases the susceptibility to developing psychopathology in adulthood.

Its relevance and importance in today’s society provides an impetus to investigate the effects of ELS on affective behaviors as well as on the amygdala, since it plays a pivotal role in fear conditioning and is critically involved in the neural circuitry mediating stress responses. While the effects of ELS on affective behaviors have been extensively studied, remarkably little is known about the effects of ELS on amygdala, although there are substantial evidences showing functional and anatomical defects of amygdala triggered by other stressors, such as chronic immobilization and predator stress. These studies indicated that, following stress, amygdala undergoes morphological changes that are apparent at multiple levels of neural organization, which together contribute to amygdala hypertrophy. Moreover, these studies also correlated the stress-induced amygdala hypertrophy with enhanced anxiogenic behaviors and highlighted the endurance of amygdala hypertrophy even after the removal of stressor. Henceforth, these suggest that the alterations in affective behaviors succeeding ELS is likely to be due to modulations in amygdala morphologies and also emphasize the potential lasting adverse effects of ELS on individuals.