Prenatal stress

Prenatal stress (or prenatal maternal stress) is exposure of an expectant mother to stress, which can be caused by stressful life events or by environmental hardships. The resulting changes to the mother's hormonal and immune system may harm the fetus's (and after birth, the infant's) immune function and brain development.

Prenatal stress is shown to have several affects in fetal brain development. In the hippocampus of adult male rats, prenatal stress has shown to decrease the rate of proliferation and cell death in the hypothalamus-pituitary axis. Prenatal stressed animals have prolonged corticosterone response. Removing the adrenal glands of the mother eliminates the effect of the pup's corticosterone response. Supplementing the adrenalectamized mother with corticosterone, rescued the hypothalamic-pituitary-axis response to maternal stress for prenatally stressed offspring. Prenatal stress caused high glucocorticoids, which in turn affects the hypothalamic-pituitary-axis negative feedback. A study by García-Cáceres et al. showed that prenatal stress decreases cell turnover and proliferation in the hypothalamus of adult rats, which reduces structural plasticity and reduces the response to stress in adulthood. This study also showed that when prenatally stressed rats were stressed in adulthood the females showed an increase in corticotropin-releasing hormone suggesting it to be an up-regulation in the hypothalamic-pituitary adrenal axis. Males showed no elevation of corticosterone levels. Increase in adrenocorticotropic hormone with no effect of adult stress and a decrease in the corticotropin-releasing hormone mRNA in the hypothalamus showed a down-regulation. The author concludes that this makes prenatally stressed females less reactive to later life stressors than males.

Pups that underwent prenatal stress showed lower plasma testosterone when compared to the control pups. This is caused by the disruption of prenatal development which did not allow the complete masculinization of the prenatally stressed pups’ central nervous system. Particularly in the striatum of the prenatally stressed male pups showed an increase in vanilmandelic acid, dopamine, serotonin, 5-hydroxyindoleacetic acid which all can affect sexual behavior. The prenatally stressed male pups showed a significant latency in mounting behavior when compared to controls. When doing the radial arm maze task prenatally stressed male rats showed a greater increase in dopamine than the prenatally stressed females, which is suggested to facilitate the impairment for the males doing the maze task, but improved the female’s performance. There was also an effect on the corticosterone secretion for prenatally stressed females. Being prenatally stressed increased the anxiety response of the female rats. Yet, it had no effect on the males.

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