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Rodent studies have revealed that the early rearing environment plays an important role in the development of stress vulnerability, memory and cognition. Although early lighting conditions (ELC) are involved in these neuronal developments through both maternal and offspring behavior, their influence has not been fully elucidated. Thus, by using Sprague-Dawley rats, we examined whether ELC affected maternal care by the dam and the subsequent neurodevelopment of the offspring. Prolonged dark phase conditions (PDC) (light/dark, 6/18 h) and prolonged light phase conditions (light/dark, 18/6 h) were administered from postnatal day 2 to postnatal day 14. Throughout this period, maternal care and the circadian rhythmicity of dams were investigated. In adolescence and adulthood of the offspring, we measured anxiety-like behavior, social interaction, object recognition memory, activity rhythm and corticosterone response to stress with hippocampal expression of N-methyl-D-aspartate and glucocorticoid receptor mRNAs. PDC altered maternal care and circadian rhythmicity in the dam compared with normal lighting conditions and prolonged light phase conditions. PDC markedly increased anxiety-like behavior, decreased social interaction and object recognition memory, and inhibited corticosterone feedback in offspring later in life. Furthermore, hippocampal levels of glucocorticoid receptor mRNA and N-methyl-D-aspartate receptor 2B mRNA in rats subjected to PDC were significantly lower than in animals subjected to normal lighting conditions. In the adult offspring, the circadian rhythm of locomotor activity was not affected. These findings suggested that ELC affect mother-infant interactions and subsequently at least partially alter the neurobehavioral development of offspring.

BackgroundIt is known that the onset, progression, and prognosis of major depressive disorder are affected by interactions between a number of factors. This study investigated how childhood abuse, personality, and stress of life events were associated with symptoms of depression in depressed people.MethodsPatients with major depressive disorder (N = 113, 58 women and 55 men) completed the Beck Depression Inventory-II (BDI-II), the Neuroticism Extroversion Openness Five Factor Inventory (NEO-FFI), the Child Abuse and Trauma Scale (CATS), and the Life Experiences Survey (LES), which are self-report scales. Results were analyzed with correlation analysis and structural equation modeling (SEM), by using SPSS AMOS 21.0.ResultsChildhood abuse directly predicted the severity of depression and indirectly predicted the severity of depression through the mediation of personality. Negative life change score of the LES was affected by childhood abuse, however it did not predict the severity of depression.ConclusionsThis study is the first to report a relationship between childhood abuse, personality, adulthood life stresses and the severity of depression in depressed patients. Childhood abuse directly and indirectly predicted the severity of depression. These results suggest the need for clinicians to be receptive to the possibility of childhood abuse in patients suffering from depression.SEM is a procedure used for hypothesis modeling and not for causal modeling. Therefore, the possibility of developing more appropriate models that include other variables cannot be excluded.

BackgroundAmygdala hyper-reactivity is sometimes assumed to be a vulnerability factor that predates depression; however, in healthy people, who experience early life stress but do not become depressed, it may represent a resilience mechanism. We aimed to test these hypothesis examining whether increased amygdala activity in association with a history of early life stress (ELS) was negatively or positively associated with depressive symptoms and impact of negative life event stress in never-depressed adults.MethodsTwenty-four healthy participants completed an individually tailored negative mood induction task during functional magnetic resonance imaging (fMRI) assessment along with evaluation of ELS.ResultsMood change and amygdala reactivity were increased in never-depressed participants who reported ELS compared to participants who reported no ELS. Yet, increased amygdala reactivity lowered effects of ELS on depressive symptoms and negative life events stress. Amygdala reactivity also had positive functional connectivity with the bilateral DLPFC, motor cortex and striatum in people with ELS during sad memory recall.ConclusionsIncreased amygdala activity in those with ELS was associated with decreased symptoms and increased neural features, consistent with emotion regulation, suggesting that preservation of robust amygdala reactions may reflect a stress buffering or resilience enhancing factor against depression and negative stressful events.

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