Abstract

Studies have documented the detrimental impact of gestational and postpartum maternal stress on the developing offspring. In susceptible individuals, stress has been associated with everything from brain developmental delays to emotionality and behavior disorders. Understanding the genetics and developmental window of greatest stress sensitivity is vital to providing the best preventative care and therapeutic targets. Corticotropin-releasing factor (CRF) and its receptors (CRFR1 and CRFR2) are the key regulators of the endocrine stress response and are critical in maintenance of organismal homeostasis. Dysregulation of these stress pathways can result in an increased sensitivity to stress. Mice deficient for CRFR2 show such a dysregulation and have been found to be a valuable genetic model of increased stress sensitivity. Initial comparisons utilizing this mouse model in studies examining maternal behaviors and cross-fostering outcome validate the complex nature– nurture contribution. Using this model, altered stress responsivity in offspring appears to require both a genetic predisposition to stress sensitivity and a postnatal environment that influences it.

Full Text
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