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The developmental impact of prenatal stress, prenatal dexamethasone and postnatal social stress on physiology, behaviour and neuroanatomy of primate offspring: studies in rhesus macaque and common marmoset.

Pryce CR, Aubert Y, Maier C, Pearce PC, Fuchs E - Psychopharmacology (Berl.) (2010)

Bottom Line: Prenatal DEX was without effect on HPA activity and reduced social play and skilled motor behaviour in marmoset.Perinatal stress-related environmental events exert short- and long-term effects on HPA function, behaviour and brain status in rhesus macaque and common marmoset.The mechanisms mediating the enduring effects remain to be elucidated, with candidates including increased basal HPA function and epigenetic programming.

View Article: PubMed Central - PubMed

Affiliation: Behavioural Neurobiology Laboratory, Swiss Federal Institute of Technology Zürich, Schwerzenbach, Switzerland.

ABSTRACT

Rationale: Exposure of the immature mammalian brain to stress factors, including stress levels of glucocorticoids, either prenatally or postnatally, is regarded as a major regulatory factor in short- and long-term brain function and, in human, as a major aetiological factor in neuropsychiatric disorders. Experimental human studies are not feasible and animal studies are required to demonstrate causality and elucidate mechanisms. A number of studies have been conducted and reviewed in rodents but there are relatively few studies in primates.

Objectives: Here we present an overview of our published studies and some original data on the effects of: (1) prenatal stress on hypothalamic-pituitary-adrenal (HPA) re/activity and hippocampus neuroanatomy in juvenile-adolescent rhesus macaques; (2) prenatal dexamethasone (DEX) on HPA activity, behaviour and prefrontal cortex neuroanatomy in infant-adolescent common marmosets; (3) postnatal daily parental separation stress on HPA re/activity, behaviour, sleep and hippocampus and prefrontal cortex neuroanatomy in infant-adolescent common marmoset.

Results: Prenatal stress increased basal cortisol levels and reduced neurogenesis in macaque. Prenatal DEX was without effect on HPA activity and reduced social play and skilled motor behaviour in marmoset. Postnatal social stress increased basal cortisol levels, reduced social play, increased awakening and reduced hippocampal glucocorticoid and mineralocorticoid receptor expression in marmoset.

Conclusions: Perinatal stress-related environmental events exert short- and long-term effects on HPA function, behaviour and brain status in rhesus macaque and common marmoset. The mechanisms mediating the enduring effects remain to be elucidated, with candidates including increased basal HPA function and epigenetic programming.

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Related in: MedlinePlus

Effects of prenatal stress, both early (EPNS) and late (LPNS) in pregnancy on behaviour, cortisol titres in basal condition and after DEX stimulation, on neurogenesis and hippocampal volume in rhesus macaque offspring generated from stressed and control pregnancies. Values are mean ± SEM; *p < 0.05, significantly different from control monkeys (with modifications from Coe et al. 2003)
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Fig2: Effects of prenatal stress, both early (EPNS) and late (LPNS) in pregnancy on behaviour, cortisol titres in basal condition and after DEX stimulation, on neurogenesis and hippocampal volume in rhesus macaque offspring generated from stressed and control pregnancies. Values are mean ± SEM; *p < 0.05, significantly different from control monkeys (with modifications from Coe et al. 2003)

Mentions: The behavioural, endocrine and neuroanatomical data are summarised in Fig. 2: Juvenile subjects from the early stress pregnancies performed significantly less exploration than controls. To characterise the activity of the HPA axis, plasma cortisol levels were determined under basal conditions and after a 12 h overnight dexamethasone treatment (DEX) at the age of 2.0–2.5 years. Rhesus monkeys from the early stress and late stress pregnancies had significantly higher basal cortisol levels than controls. Twelve hours after DEX administration, both the early stress and late stress monkeys had significantly higher cortisol levels than controls, suggesting that their HPA axis was relatively insensitive to DEX suppression which, given the low blood–brain barrier permeability of DEX, would be expected to be exerted primarily at the level of the glucocorticoid receptors expressed by the pituitary gland. Clearly, the experience of maternal stress during pregnancy results in the offspring having a different set point for the HPA axis. In turn, these findings indicate that chronic changes in adrenocortical hormone levels could be involved in mediating the chronic maternal stress effects on the offspring (Dodic et al. 2002; Nyirenda and Seckl 1998; Wadhwa et al. 2001).Fig. 2


The developmental impact of prenatal stress, prenatal dexamethasone and postnatal social stress on physiology, behaviour and neuroanatomy of primate offspring: studies in rhesus macaque and common marmoset.

Pryce CR, Aubert Y, Maier C, Pearce PC, Fuchs E - Psychopharmacology (Berl.) (2010)

Effects of prenatal stress, both early (EPNS) and late (LPNS) in pregnancy on behaviour, cortisol titres in basal condition and after DEX stimulation, on neurogenesis and hippocampal volume in rhesus macaque offspring generated from stressed and control pregnancies. Values are mean ± SEM; *p < 0.05, significantly different from control monkeys (with modifications from Coe et al. 2003)
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3045510&req=5

Fig2: Effects of prenatal stress, both early (EPNS) and late (LPNS) in pregnancy on behaviour, cortisol titres in basal condition and after DEX stimulation, on neurogenesis and hippocampal volume in rhesus macaque offspring generated from stressed and control pregnancies. Values are mean ± SEM; *p < 0.05, significantly different from control monkeys (with modifications from Coe et al. 2003)
Mentions: The behavioural, endocrine and neuroanatomical data are summarised in Fig. 2: Juvenile subjects from the early stress pregnancies performed significantly less exploration than controls. To characterise the activity of the HPA axis, plasma cortisol levels were determined under basal conditions and after a 12 h overnight dexamethasone treatment (DEX) at the age of 2.0–2.5 years. Rhesus monkeys from the early stress and late stress pregnancies had significantly higher basal cortisol levels than controls. Twelve hours after DEX administration, both the early stress and late stress monkeys had significantly higher cortisol levels than controls, suggesting that their HPA axis was relatively insensitive to DEX suppression which, given the low blood–brain barrier permeability of DEX, would be expected to be exerted primarily at the level of the glucocorticoid receptors expressed by the pituitary gland. Clearly, the experience of maternal stress during pregnancy results in the offspring having a different set point for the HPA axis. In turn, these findings indicate that chronic changes in adrenocortical hormone levels could be involved in mediating the chronic maternal stress effects on the offspring (Dodic et al. 2002; Nyirenda and Seckl 1998; Wadhwa et al. 2001).Fig. 2

Bottom Line: Prenatal DEX was without effect on HPA activity and reduced social play and skilled motor behaviour in marmoset.Perinatal stress-related environmental events exert short- and long-term effects on HPA function, behaviour and brain status in rhesus macaque and common marmoset.The mechanisms mediating the enduring effects remain to be elucidated, with candidates including increased basal HPA function and epigenetic programming.

View Article: PubMed Central - PubMed

Affiliation: Behavioural Neurobiology Laboratory, Swiss Federal Institute of Technology Zürich, Schwerzenbach, Switzerland.

ABSTRACT

Rationale: Exposure of the immature mammalian brain to stress factors, including stress levels of glucocorticoids, either prenatally or postnatally, is regarded as a major regulatory factor in short- and long-term brain function and, in human, as a major aetiological factor in neuropsychiatric disorders. Experimental human studies are not feasible and animal studies are required to demonstrate causality and elucidate mechanisms. A number of studies have been conducted and reviewed in rodents but there are relatively few studies in primates.

Objectives: Here we present an overview of our published studies and some original data on the effects of: (1) prenatal stress on hypothalamic-pituitary-adrenal (HPA) re/activity and hippocampus neuroanatomy in juvenile-adolescent rhesus macaques; (2) prenatal dexamethasone (DEX) on HPA activity, behaviour and prefrontal cortex neuroanatomy in infant-adolescent common marmosets; (3) postnatal daily parental separation stress on HPA re/activity, behaviour, sleep and hippocampus and prefrontal cortex neuroanatomy in infant-adolescent common marmoset.

Results: Prenatal stress increased basal cortisol levels and reduced neurogenesis in macaque. Prenatal DEX was without effect on HPA activity and reduced social play and skilled motor behaviour in marmoset. Postnatal social stress increased basal cortisol levels, reduced social play, increased awakening and reduced hippocampal glucocorticoid and mineralocorticoid receptor expression in marmoset.

Conclusions: Perinatal stress-related environmental events exert short- and long-term effects on HPA function, behaviour and brain status in rhesus macaque and common marmoset. The mechanisms mediating the enduring effects remain to be elucidated, with candidates including increased basal HPA function and epigenetic programming.

Show MeSH
Related in: MedlinePlus