Zusammenfassung
We studied the mechanisms of genetic-early environmental interactions to modulate adult stress-coping and tested the hypothesis that prenatal stress (PS) can differentially alter the consequences of a genetic predisposition to either hyper- or hypo-anxiety. Exposure of male Wistar rats, bred for high (HAB) or low (LAB) anxiety-related behaviour, to PS between pregnancy days 4 and 18 resulted in ...
Zusammenfassung
We studied the mechanisms of genetic-early environmental interactions to modulate adult stress-coping and tested the hypothesis that prenatal stress (PS) can differentially alter the consequences of a genetic predisposition to either hyper- or hypo-anxiety. Exposure of male Wistar rats, bred for high (HAB) or low (LAB) anxiety-related behaviour, to PS between pregnancy days 4 and 18 resulted in opposite effects on anxiety in adulthood, i.e. HAB rats became less and LAB rats became more anxious compared with their unstressed controls (plus-maze and holeboard). The high anxiety of HAB controls was accompanied by elevated expression of vasopressin and corticotropin-releasing hormone (CRH) mRNA within the hypothalamic paraventricular nucleus compared with LAB rats. PS reduced CRH mRNA expression in HAB rats but increased vasopressin mRNA expression in LAB rats, which may explain the opposite effects of PS on adult emotionality. Differential effects of PS were also found with respect to hypothalamo-pituitary-adrenal axis reactivity; the hypothalamo-pituitary-adrenal hyper-response in virgin female HAB controls became attenuated after PS, without affecting plasma corticosterone concentrations in LAB rats. Differences in maternal plasma corticosterone measured between pregnancy days 6 and 14 of HAB and LAB dams or differential effects of PS on maternal behaviour can be excluded. In conclusion, exposure of rats with genetically determined high or low emotionality to PS mitigates the extremes in behavioural and neuroendocrine stress-coping, thus allowing adequate and similar behavioural responses to potentially dangerous stimuli in adulthood. Differential effects of PS on the activity of the brain vasopressin and CRH systems might represent possible underlying molecular mechanisms.
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