Effects of prenatal stress on developmental anatomy of the brain and adult behavioural pathology

Abstract

Perinatal period is a time of particular vulnerability to stress which has serious consequences on the developing foetus through both maternal behaviours and physiological changes. Such distress can result from natural or man-made disasters such as earthquakes, floods, storms, war or terrorist acts. Besides, not only in socio-economically disadvantaged regions with less educated background and high unemployment rates, but also in every civilized society; pregnant women are exposed to intimate partner and patriarchal family violence, as well as interpersonal tensions or adverse conditions in the workplace.1 Moreover, pregnancy related risk factors and dramatic fluctuations in gonadal hormone levels increase the prevalence of mood disorders and anxiety symptoms during this period. 2-4 Regardless of its nature and origin, stressful situations are considered as a 'threat to homeostasis' and a series of morphological, physiological and behavioural responses occur to restore the original condition. 5 Unfortunately, these responses negatively affect the rate of development, mental and physical health of the offspring and increase the incidence of preterm birth, lower birth weights and smaller head circumferences.6-8In turn, less optimal birth outcomes can lead to longterm cognitive impairments and motor disabilities.There is also compelling evidence showing that stress exposure during prenatal life enhances susceptibility for emotional problems and behavioural disorders later in Effects of prenatal stress on developmental anatomy of the brain and adult behavioural pathology Emel Ulup›nar Department of Anatomy, Faculty of Medicine, Eskiflehir Osmangazi University, Turkey AbstractDuring critical or sensitive periods of development, the brain is highly plastic and particularly vulnerable to environmental adverse effects, including stress. In response to gestational stress, activation of the sympathetic system, the HPA axis and the central limbic stress loop increase the level of circulating glucocorticoids and catecholamines in both mother and foetus. Exposure to the excess amount of corticosteroids permanently reduces the glucocorticoid and mineralocorticoid receptors; thereby leading to an attenuation of the HPA axis feedback sensitivity and enhanced responsiveness to stress in the adult offspring. In the assessment of consequences at the behavioural, functional, and morphological levels; experimental animal models of maternal stress are extremely useful, in which the timing, intensity and duration of stress exposure can be readily controlled. These animal studies have revealed important links between prenatal stress exposure, life-long changes in the HPA function, and enhanced risk for subsequent psychopathology in a sex-specific manner. The aim of this review is to examine the impacts of prenatal stress on developmental anatomy of the brain, particularly focusing on the relevant emotional and behavioural outcomes within the context of current data obtained from experimental animals.

Placental CRH as a Signal of Pregnancy Adversity and Impact on Fetal Neurodevelopment

“…Optimal function of this adaptation process ( 2 ), involving mediators of the neuroendocrine stress response, promotes brain plasticity and resilience. In cases of excessive prenatal adversity, optimal homeostatic equilibrium might be severely impaired ( 3 ) and (mal)adaptive responses might contribute to development of prolonged pathogenic mechanisms. Pathological signals arising from the mother can be transmitted to the developing fetus leading to adverse programming of the offspring ( 2 , 4 ).…”

Investigating the gut-brain axis in a neurodevelopmental rodent model of schizophrenia

“…This is in line with our previous findings of increased expression levels of CRHR1 mRNA in adulthood following neonatal infection that correlate with increased glucocorticoid receptor mRNA levels, without changes in CRH mRNA expression ( Sominsky et al., 2013 ). The interaction of glucocorticoids and CRH with their respective receptors during critical periods of brain maturation can alter the programing of the HPA axis ( Ulupınar, 2009 ) with studies suggesting that CRHR1 is essential in mediating behavioural responses to stress and susceptibility to neuropathology. Alterations in this receptor in female adolescents following MIA-ACE as found in this study may indicate downstream alterations or exacerbations in schizophrenia-related behaviours such as sensorimotor gating deficits, sensitivity to psychomimetic drugs, and working memory impairments.…”

L’exposition Aux Contaminants Environnementaux Comme Un Facteur De Risque Au Développement Des Troubles Intériorisés

“…Des travaux réalisés chez l'animal montrent que le développement ontogénétique de l'hippocampe succède à celui de l'amygdale, ce qui pourrait expliquer, par une série d'évènements en cascade, que les anomalies de l'hippocampe contribuant aux troubles intériorisés à la suite d'un stress prénatal deviennent apparentes seulement à la fin de l'adolescence (Andersen et al, 2008;Tottenham & Sheridan, 2010). L'essentiel de la structure et du fonctionnement de l'amygdale se développe prénatalement, mais continue aussi à se développer et à s'affiner jusqu'à l'âge adulte, avec un sommet d'activation lors de l'adolescence et diminuant ensuite à l'âge adulte, ce qui serait lié avec le développement du cortex préfrontal ventromédian à l'adolescence (Ulupinar, 2009;Tottenham & Sheridan, 2010). Ainsi, l'adolescence constitue une autre fenêtre de vulnérabilité majeure dans le développement du circuit neuronal de la peur, particulièrement en ce qui concerne les régions préfrontales.…”