Abstract
Early-life adverse experiences (first hit) lead to coping strategies that may confer resilience or vulnerability to later experienced stressful events (second hit) and the subsequent development of stress-related psychopathologies. Here, we investigated whether exposure to two stressors at different stages in life has long-term effects on emotional and cognitive capabilities, and whether the interaction between the two stressors influences stress resilience. Male rats were subjected to social defeat stress (SDS, first hit) in adolescence and to a single episode of prolonged stress (SPS, second hit) in adulthood. Behavioral outcomes, hippocampal expression of brain-derived neurotrophic factor, and plasma corticosterone levels were tested in adulthood. Rats exposed to both stressors exhibited resilience against the development of stress-induced alterations in emotional behaviors and spatial memory, but vulnerability to cued fear memory dysfunction. Rats subjected to both stressors demonstrated resilience against the SDS-induced alterations in hippocampal brain-derived neurotrophic factor expression and plasma corticosterone levels. SPS alone altered locomotion and spatial memory retention; these effects were absent in SDS-exposed rats later exposed to SPS. Our findings reveal that exposure to social stress during early adolescence influences the ability to cope with a second challenge experienced later in life.
Highlights
Stress exposure can lead to the development of several psychiatric diseases, including anxiety, depression, and post-traumatic stress disorder (PTSD) [1,2]
These results indicate that exposure to social defeat stress (SDS) during early adolescence induced an increase in Brain-derived neurotrophic factor (BDNF) protein expression in the hippocampus of adult rats, while single prolonged stress (SPS) did not
The present findings indicate that exposure to social stress during early adolescence influences the ability to cope with a second challenge experienced later in life
Summary
Stress exposure can lead to the development of several psychiatric diseases, including anxiety, depression, and post-traumatic stress disorder (PTSD) [1,2]. Early-life stressful experiences may lead to coping strategies that match or mismatch later-life adverse experiences, resulting in resilience or vulnerability, respectively, to the development of psychopathologies in adulthood [3,4,5,6]. Because adolescence is a crucial developmental stage associated with profound changes in the structure and function of the brain [7,8,9], stress experienced during this critical developmental period has more detrimental effects compared with those experienced in adulthood. Chronic glucocorticoid exposure during adolescence is associated with adverse consequences, in the hippocampus where it causes neuronal cell damage and dendritic atrophy, reduces neurogenesis, impairs synaptic plasticity, and suppresses long-term potentiation [13,14,15,16].
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