Abstract
Early-life stress causes anxiogenesis and sensitivity of stress endocrine axis, facilitated by changes in the basolateral amygdala and hippocampal neurogenesis. In this report, we examined if male-like relationship between early-life stress and anxiety was recapitulated in female rats, along with related neurobiological substrates of the amygdala and the hippocampus. Maternal separation, a paradigm consistently utilized in male rats in most previously published scripts, did not cause similar behavioral consequences in females. Maternal separation caused an increase in adult hippocampal neurogenesis in females without causing substantial differences in dendritic arbors of the basolateral amygdala. Thus, female rats displayed remarkable resilience in the emotional consequences of early-life stress.
Highlights
The quality and quantity of interactions with the mother have longterm consequences for the emotional development of the offspring
Data described in three preceding paragraphs show that maternal separation does not lead to anxiogenesis or basolateral amygdala (BLA) reorganization in adulthood in female rats
Indicative gender dimorphism in the anxiogenesis is interesting because female humans are diagnosed with anxiety disorders at much higher rates than males [13, 14]
Summary
The quality and quantity of interactions with the mother have longterm consequences for the emotional development of the offspring. Reduced maternal care or periods of maternal absence leads to a higher incidence of psychiatric disorders [1] and lower life expectancy in humans [2] This phenomenon has been repeatedly modeled in rats and mice using paradigms of maternal separation, whereby dams are intermittently separated from the pups during the pre-weaning stage [3]. Maternal separation causes sustained plasticity within the hippocampus and the amygdala [8, 9], brain regions that form crucial parts of brain circuits regulating stress endocrine response This is not surprising because the separation coincides with critical periods of brain development where brain regions exerting central control on stress responses are maturing and are open to ontogenic shifts due to changes in the maternal environment [10]
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