Prenatal stress in rats: effects on plasma corticosterone, hippocampal glucocorticoid receptors, and maze performance

Szuran, Thomas F.; Pliška, V.; Pokorny, Jana; Welzl, Hans

doi:10.1016/s0031-9384(00)00351-6

Cited by 236 publications

(172 citation statements)

References 40 publications

Supporting

Mentioning

147

Contrasting

Unclassified

Order By: Relevance

“…Some studies in rats and also in guinea pigs indicate that programming of corticosteroid receptors, such as the HPA axis, is possibly sex-specific with the effect of prenatal glucocorticoids being larger in female offspring (Weinstock et al 1992, Dean & Matthews 1999, Szuran et al 2000, Bowman et al 2004, Gerardin et al 2005. In pigs, we found no sex-specific effects on brain GRs, but an interaction of sex and treatment on plasma CBG concentrations in 28-day-old LG-piglets.…”

Section: Acthcontrasting

confidence: 53%

Changes in endocrine and neurochemical profiles in neonatal pigs prenatally exposed to increased maternal cortisol

Kanitz¹,

Otten²,

Tuchscherer³

2006

Journal of Endocrinology

View full text Add to dashboard Cite

Early life environmental factors are able to influence prenatal development and may cause structural and functional effects on hypothalamic-pituitary-adrenal (HPA) axis and neurotransmitter systems in the offspring. These effects seem to be species specific and may depend on the period of gestation when the factors are effective. Elevated maternal cortisol levels are assumed to play a crucial role as a programming factor during prenatal development. Thus, the present study was performed in order to examine the effects of increased maternal cortisol levels during mid-and late gestation on central and peripheral alterations of the HPA axis and brain neurotransmitter profiles in piglets. Endogenous cortisol release was induced by i.m. administration of ACTH to sows every second day either during mid-(day 49 until 75) or late gestation (day 85 until 107). Controls received injections of saline. ACTH treatment of sows during mid-and late gestation had no effects on the gestation length, the number of total born and the frequency of stillborn piglets. However, ACTH treatment during late gestation caused an increase of birth weight (P!0$04) and affected the organ:body weight ratios (brain and adrenal) in the offspring. There was an impact of increased maternal cortisol on the HPA axis and on central neurotransmitter systems in the offspring. ACTH treatment during mid gestation caused a significant decrease of plasma corticosteroid-binding globulin (CBG; P!0$03) and an increase of the noradrenergic activity in the locus coeruleus (LC) region (P!0$02). Elevated maternal cortisol during late gestation also produced a significant decrease of plasma CBG (P!0$05), but significantly increased the plasma noradrenaline (NA) concentration (P!0$02) and decreased the serotonergic activity in the LC at both postnatal day 1 (P!0$016) and day 28 (P!0$003). Furthermore, there were sex-specific effects of ACTH treatment on plasma CBG, NA and brain monoamine turnover, with more pronounced changes in male offspring. In conclusion, elevated maternal cortisol levels during mid-and late gestation in pigs affect growth, HPA axis and brain neurotransmitter systems in the offspring in a sex-specific manner. The observed alterations in endocrine and neurotransmitter systems are dependent on the gestational period. Late gestation appears to be a more sensitive phase for cortisol-induced programming in pigs. Moreover, the present data show that there are marked developmental differences between laboratory animals and domestic pigs, and highlight the importance of speciesspecific studies on prenatal influences.

show abstract

Section: Acthcontrasting

confidence: 53%

Changes in endocrine and neurochemical profiles in neonatal pigs prenatally exposed to increased maternal cortisol

Kanitz¹,

Otten²,

Tuchscherer³

2006

Journal of Endocrinology

View full text Add to dashboard Cite

show abstract

“…Changes in levels of 5-HT and metabolites have been reported in response to prenatal stress, as have behavioral changes in response to administration of serotonergic compounds (Ishiwata et al 2005). Maternal Pb exposure per se has also been shown, in some studies, to influence levels of serotonergic compounds (Szuran et al 2000;Cory-Slechta et al 2004). Thus, a potential role for 5HT in the effects of Pb/stress on FI response rates is interesting to consider, and changes in levels of 5-HT and 5-HIAA were seen almost uniformly across regions in both genders.…”

Section: Discussionmentioning

confidence: 99%

“…Maternal stress has profound and enduring consequences for multiple systems of offspring, altering endocrine, behavioral, cardiovascular and metabolic regulation Seckl 2004;Seckl and Meaney 2004;Seckl and Holmes 2007). For the central nervous system, effects include changes in learning and memory and other behavioral dysfunctions (Lemaire et al 2000;Lordi et al 2000;Meek et al 2000;Szuran et al 2000;Fumagalli et al 2007). Importantly, some of these consequences of maternal stress have now been shown to be transgenerational (Kapoor et al 2006;Seckl and Meaney 2006;Seckl and Holmes 2007).…”

Section: Introductionmentioning

confidence: 99%

CNS effects of developmental Pb exposure are enhanced by combined maternal and offspring stress

et al. 2008

View full text Add to dashboard Cite

Lead (Pb) exposure and elevated stress are co-occurring risk factors. Both impact brain mesolimbic dopamine/glutamate systems involved in cognitive functions. We previously found that maternal stress can potentiate Pb-related adverse effects in offspring at blood Pb levels averaging approximately 40 ug/dl. The current study of combined Pb exposure and stress sought to extend those results to lower levels of Pb exposure, and to examine relationships among consequences in offspring for Fixed Interval (FI) schedule-controlled behavior, neurochemistry and corticosterone levels. Dams were exposed to maternal Pb beginning 2 mos prior to breeding (0, 50 or 150 ppm in drinking water), maternal restraint stress on gestational days 16 and 17 (MS), or the combination. In addition, a subset of offspring from each resultant treatment group was also exposed intermittently to variable stressors as adults (MS+OS). Marked "Pb-stress"-related increases in response rates on a Fixed Interval schedule, a behavioral performance with demonstrated sensitivity to Pb, occurred preferentially in female offspring even at mean blood Pb levels of 11 ug/dl when 50 ppm Pb was combined with maternal and offspring stress. Greater sensitivity of females to frontal cortex catecholamine changes may contribute to the elevated FI response rates as mesocorticolimbic systems are critical to the mediation of this behavior. Basal and final corticosterone levels of offspring used to evaluate FI performance differed significantly from those of non-behaviorally tested (NFI) littermates, demonstrating that purported mechanisms of Pb, stress or Pb/stress effects determined in nonbehaviorally trained animals cannot necessarily be generalized to animals with behavioral histories. Finally, the persistent and permanent consequences of Pb, stress and Pb+stress in offspring of both genders suggest that Pb screening programs should include pregnant women at risk for elevated Pb exposure, and that stress should be considered as an additional risk factor. Pb+stress effects observed in the absence of either risk factor alone (i.e., potentiated effects) raise questions about the capacity of current hazard identification approaches to adequately identify human health risks posed by neurotoxicants.

show abstract

“…Women are more likely than men to develop depression following a stressful life event early in life 300 and their HPA axis is more susceptible to PS-induced programming. [301][302][303] Women have a lower mean rate of 5-HT synthesis compared to men, while men and women appear to have similar stores of brain 5-HT. 109 Thus, in times of increased 5-HT utilization, a lower rate of synthesis in women may cause 5-HT levels to decline more in women than in men, possibly increasing vulnerability to depression.…”

Section: Biopsychological Interactionsmentioning

confidence: 99%

Serotonergic vulnerability and depression: assumptions, experimental evidence and implications

et al. 2006

View full text Add to dashboard Cite

In recent years, the term serotonergic vulnerability (SV) has been used in scientific literature, but so far it has not been explicitly defined. This review article attempts to elucidate the SV concept. SV can be defined as increased sensitivity to natural or experimental alterations of the serotonergic (5-HTergic) system. Several factors that may disrupt the 5-HTergic system and hence contribute to SV are discussed, including genetic factors, female gender, personality characteristics, several types of stress and drug use. It is explained that SV can be demonstrated by means of manipulations of the 5-HTergic system, such as 5-HT challenges or acute tryptophan depletion (ATD). Results of 5-HT challenge studies and ATD studies are discussed in terms of their implications for the concept of SV. A model is proposed in which a combination of various factors that may compromise 5-HT functioning in one person can result in depression or other 5-HT-related pathology. By manipulating 5-HT levels, in particular with ATD, vulnerable subjects may be identified before pathology initiates, providing the opportunity to take preventive action. Although it is not likely that this model applies to all cases of depression, or is able to identify all vulnerable subjects, the strength of the model is that it may enable identification of vulnerable subjects before the 5-HT related pathology occurs. Molecular Psychiatry ( Keywords: serotonin; mood disorders; stress; genetics; sex; tryptophan Involvement of serotonin in depressionMood disorders are one of the most prevalent forms of mental illness. 1 According to the DSM-IV, the lifetime risk for major depressive disorder is between 10 and 25% for women and between 5 and 12% for men. 2 Depression has been studied intensively during the last few decades, but the psychological and neurobiological determinants of depression have not yet been precisely defined. Although several factors are known to contribute to the etiology of depression, it is not clear how these factors cause depression, and why some subjects become depressed while others remain unaffected. In terms of biological factors in the etiology of depression, there are several hypotheses. These include neurotransmitter dysfunctions (serotonin, 5-HT; dopamine, DA; norepinephrine, NE); dysregulations in hypothalamic-pituitary-adrenal (HPA) axis activity; and immune system imbalance. The aim of this article is not to discuss all of these hypotheses in detail, but to evaluate the role that serotonin may play within these hypothesized mechanisms.It is widely accepted that diminished serotonergic (5-HTergic) function is involved in the onset and course of depression. 3,4 The 5-HTergic system is a large and complex system. Although nearly all cell bodies of 5-HTergic neurons are located in the raphe nuclei in the brain stem, the axons of these neurons innervate almost the entire brain. The actions of 5-HT are mediated by 16 types and subtypes of receptors. 5 As the 5-HTergic system is assumed to be a modulatory system, the exact func...

show abstract

Prenatal stress in rats: effects on plasma corticosterone, hippocampal glucocorticoid receptors, and maze performance

Cited by 236 publications

References 40 publications

Changes in endocrine and neurochemical profiles in neonatal pigs prenatally exposed to increased maternal cortisol

Changes in endocrine and neurochemical profiles in neonatal pigs prenatally exposed to increased maternal cortisol

CNS effects of developmental Pb exposure are enhanced by combined maternal and offspring stress

Serotonergic vulnerability and depression: assumptions, experimental evidence and implications

Contact Info

Product

Resources

About