Early-life stress is associated with a high prevalence of mental illnesses such as post-traumatic stress disorders, attention-deficit/hyperactivity disorder, schizophrenia, and anxiety or depressive behavior, which constitute major public health problems. In the early stages of brain development after birth, events such as synaptogenesis, neuron maturation, and glial differentiation occur in a highly orchestrated manner, and external stress can cause adverse long-term effects throughout life. Our body utilizes multifaceted mechanisms, including neuroendocrine and neurotransmitter signaling pathways, to appropriately process external stress. Newborn individuals first exposed to early-life stress deploy neurogenesis as a stress-defense mechanism; however, in adulthood, early-life stress induces apoptosis of mature neurons, activation of immune responses, and reduction of neurotrophic factors, leading to anxiety, depression, and cognitive and memory dysfunction. This process involves the hypothalamus-pituitary-adrenal axis and neurotransmitters secreted by the central nervous system, including norepinephrine, dopamine, and serotonin. The rodent early-life stress model is generally used to experimentally assess the effects of stress during neurodevelopment. This paper reviews the use of the early-life stress model and stress response mechanisms of the body and discusses the experimental results regarding how early-life stress mediates stress-related pathways at a high vulnerability of psychiatric disorder in adulthood.
Keywords: early-life stress; hypothalamic-pituitary-adrenergic axis; maternal separation; mental illness; neurodevelopmental disorder; neuroendocrine system; neurotransmitter.