Effects of repeated maternal stress on FOS expression in the hypothalamic paraventricular nucleus of fetal rats

Tobe, Ikuyo; Ishida, Yoshiteru; Tanaka, Masuo; Endoh, Hisashi; Fujioka, Takashi; Nakamura, Shôji

doi:10.1016/j.neuroscience.2005.04.023

Cited by 33 publications

(21 citation statements)

References 24 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…On the structural level, previous work has indicated that PS increases apoptosis in the fetal hypothalamus (Fujioka et al, 1999; Tobe et al, 2005), but decreases apoptosis in adulthood (Baquedano et al, 2011). Although MS was not found to affect local neuronal density during the SHRP, it increased neuronal density afterwards, which was joined by decreased levels of apoptosis-stimulating proteins and enzymes, whilst cell survival-stimulating protein levels were increased (Irles et al, 2014).…”

Section: Hpa-axis Programming By Early Life Stress (Els)mentioning

confidence: 99%

“…Prenatally stressed (PS) females were shown to display a higher peak corticosterone plasma levels to stress in adulthood compared to males (Brunton and Russell, 2010). They display increased fetal paraventricular nucleus (PVN) apoptosis in response to acute immobilization (Tobe et al, 2005), as well as higher basal PVN CRH (though inconsistently) and arginine vasopressin mRNA expression levels (Brunton and Russell, 2010; Zohar and Weinstock, 2011), and higher basal adrenocorticotropic hormone plasma levels as a result of PS compared to males. However, females do not display a significantly higher acute stress-induced increase in POMC mRNA expression in the anterior pituitary compared to non-stressed controls, while males do (Brunton and Russell, 2010).…”

Section: Hpa-axis Programming By Early Life Stress (Els)mentioning

confidence: 99%

See 1 more Smart Citation

Modulation of the Hypothalamic-Pituitary-Adrenal Axis by Early Life Stress Exposure

Bodegom

Homberg

Henckens

2017

Front. Cell. Neurosci.

424

331

View full text Add to dashboard Cite

Exposure to stress during critical periods in development can have severe long-term consequences, increasing overall risk on psychopathology. One of the key stress response systems mediating these long-term effects of stress is the hypothalamic-pituitary-adrenal (HPA) axis; a cascade of central and peripheral events resulting in the release of corticosteroids from the adrenal glands. Activation of the HPA-axis affects brain functioning to ensure a proper behavioral response to the stressor, but stress-induced (mal)adaptation of the HPA-axis' functional maturation may provide a mechanistic basis for the altered stress susceptibility later in life. Development of the HPA-axis and the brain regions involved in its regulation starts prenatally and continues after birth, and is protected by several mechanisms preventing corticosteroid over-exposure to the maturing brain. Nevertheless, early life stress (ELS) exposure has been reported to have numerous consequences on HPA-axis function in adulthood, affecting both its basal and stress-induced activity. According to the match/mismatch theory, encountering ELS prepares an organism for similar (“matching”) adversities during adulthood, while a mismatching environment results in an increased susceptibility to psychopathology, indicating that ELS can exert either beneficial or disadvantageous effects depending on the environmental context. Here, we review studies investigating the mechanistic underpinnings of the ELS-induced alterations in the structural and functional development of the HPA-axis and its key external regulators (amygdala, hippocampus, and prefrontal cortex). The effects of ELS appear highly dependent on the developmental time window affected, the sex of the offspring, and the developmental stage at which effects are assessed. Albeit by distinct mechanisms, ELS induced by prenatal stressors, maternal separation, or the limited nesting model inducing fragmented maternal care, typically results in HPA-axis hyper-reactivity in adulthood, as also found in major depression. This hyper-activity is related to increased corticotrophin-releasing hormone signaling and impaired glucocorticoid receptor-mediated negative feedback. In contrast, initial evidence for HPA-axis hypo-reactivity is observed for early social deprivation, potentially reflecting the abnormal HPA-axis function as observed in post-traumatic stress disorder, and future studies should investigate its neural/neuroendocrine foundation in further detail. Interestingly, experiencing additional (chronic) stress in adulthood seems to normalize these alterations in HPA-axis function, supporting the match/mismatch theory.

show abstract

Section: Hpa-axis Programming By Early Life Stress (Els)mentioning

confidence: 99%

Section: Hpa-axis Programming By Early Life Stress (Els)mentioning

confidence: 99%

Modulation of the Hypothalamic-Pituitary-Adrenal Axis by Early Life Stress Exposure

Bodegom

Homberg

Henckens

2017

Front. Cell. Neurosci.

424

331

View full text Add to dashboard Cite

show abstract

“…Developmental trajectories in the brain are strongly altered by prenatal stress or high pregnancy anxiety, which leads to grey matter volume reductions in several brain areas (prefrontal cortex (PFC), hippocampus and hypothalamus) in humans 90,91 and rodents [92][93][94] . Rodent studies suggest an important role for glucocorticoid-induced apoptosis in some of these effects 95 .…”

Section: Structural Changesmentioning

confidence: 99%

Stress and the social brain: behavioural effects and neurobiological mechanisms

2015

View full text Add to dashboard Cite

“…Adult females develop anxiety- and depressive- like behaviors following maternal stress (Fride and Weinstock, 1988, Alonso et al, 1991, Keshet and Weinstock, 1995, Vallee et al, 1997, Frye and Wawrzycki, 2003, Richardson et al, 2006, Zagron and Weinstock, 2006) or overexposure to glucocorticoids (GC) (Welberg et al, 2001, Oliveira et al, 2006, Zagron and Weinstock, 2006, Nagano et al, 2008). Prenatal stress and overexposure to GC also have been shown to have a variety of sex-specific impacts on brain regions thought to be involved in stress regulation, such as the hypothalamus, amygdala, and frontal cortex (Tobe et al, 2005, Murmu et al, 2006, Zuloaga et al, 2011, Carbone et al, 2012, Zuloaga et al, 2012). These data, if applicable to the human condition, imply that developmental overexposure to GC alters brain programming in a sex selective manner, resulting in increased risk in females for developing anxiety or depressive disorder in adulthood.…”

Section: Introductionmentioning

confidence: 99%

Sex-dependent programming effects of prenatal glucocorticoid treatment on the developing serotonin system and stress-related behaviors in adulthood

et al. 2016

View full text Add to dashboard Cite

Prenatal stress and overexposure to glucocorticoids (GC) during development may be associated with an increased susceptibility to a number of diseases in adulthood including neuropsychiatric disorders, such as depression and anxiety. In animal models, prenatal overexposure to GC results in hyper-responsiveness to stress in adulthood, and females appear to be more susceptible than males. Here, we tested the hypothesis that overexposure to GC during fetal development has sex-specific programming effects on the brain, resulting in altered behaviors in adulthood. We examined the effects of dexamethasone (DEX; a synthetic GC) during prenatal life on stress-related behaviors in adulthood and on the tryptophan hydroxylase-2 (TpH2) gene expression in the adult dorsal raphe nucleus (DRN). TpH2 is the rate-limiting enzyme for serotonin (5-HT) synthesis and has been implicated in the etiology of human affective disorders. Timed-pregnant rats were treated with DEX from gestational days 18–22. Male and female offspring were sacrificed on the day of birth (postnatal day 0; P0), P7, and in adulthood (P80-84) and brains were examined for changes in TpH2 mRNA expression. Adult animals were also tested for anxiety- and depressive- like behaviors. In adulthood, prenatal DEX increased anxiety- and depressive- like behaviors selectively in females, as measured by decreased time spent in the center of the open field and increased time spent immobile in the forced swim test, respectively. Prenatal DEX increased TpH2 mRNA selectively in the female caudal DRN at P7, whereas it decreased TpH2 mRNA selectively in the female caudal DRN in adulthood. In animals challenged with restraint stress in adulthood, TpH2 mRNA was significantly lower in rostral DRN of prenatal DEX treated females compared to vehicle treated females. These data demonstrated that prenatal overexposure to GC alters the development of TpH2 gene expression and these alterations correlated with lasting behavioral changes found in adult female offspring.

show abstract

Effects of repeated maternal stress on FOS expression in the hypothalamic paraventricular nucleus of fetal rats

Cited by 33 publications

References 24 publications

Modulation of the Hypothalamic-Pituitary-Adrenal Axis by Early Life Stress Exposure

Modulation of the Hypothalamic-Pituitary-Adrenal Axis by Early Life Stress Exposure

Stress and the social brain: behavioural effects and neurobiological mechanisms

Sex-dependent programming effects of prenatal glucocorticoid treatment on the developing serotonin system and stress-related behaviors in adulthood

Contact Info

Product

Resources

About