Effects of stress and adrenocorticotrophin administration on plasma corticosterone levels at different stages of pregnancy in the mouse

Barlow, Susan; Quyyumi, AA; Rajaratnam, D.; Sullivan, Frank

doi:10.1007/bf01937447

Cited by 11 publications

(5 citation statements)

References 6 publications

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“…The late pregnant mice had greatly elevated basal plasma total corticosterone concentrations compared with all other groups studied, and this has also been reported as early as d 12 in pregnancy (1,37). We now show that at the end of pregnancy, this does not reflect an increased basal plasma ACTH concentration, indicating a dissociation between basal ACTH and corticosterone and enhanced adrenal sensitivity to circulating ACTH (38), as found in other species at the end of pregnancy [rat (4,39), human (40), and sheep (41)]. …”

Section: Basal and Stress-induced Activity Of The Hpa Axis In Pregnansupporting

confidence: 70%

Neuroendocrine Responses to Stress in Mice: Hyporesponsiveness in Pregnancy and Parturition

Brunton²,

et al. 2003

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Hypothalamo-pituitary-adrenal axis secretory responses to stress were compared in female virgin, late pregnant, parturient, and lactating mice. The basal plasma ACTH concentration was not different in pregnancy or lactation compared with virgins, but corticosterone concentration and corticosteroid-binding globulin capacity were greatly elevated in late pregnancy. Secretory responses to novel environment were attenuated in pregnant, but not lactating, mice compared with virgin females, whereas ACTH responses to forced swimming were attenuated in both groups. The expression of immediate early gene (nur77) mRNA increased in paraventricular nucleus neurons after stress exposure in virgin and lactating, but not pregnant, mice. During parturition, the basal ACTH concentration was similar to virgin and pregnant controls and did not increase with stress. Oxytocin secretion in response to either novel environment or forced swimming was unchanged in any reproductive group, whereas vasopressin secretion was decreased by both stressors, but only in virgins. Pretreatment with oxytocin receptor antagonist centrally had no effect on ACTH responses to stress in either virgin or pregnant mice. Pretreatment with an opioid receptor antagonist increased ACTH responses to stress in virgin mice, indicating opioid inhibition, but had no effect in pregnancy. Thus, in mice hypothalamo-pituitary-adrenal hyporesponsiveness in late pregnancy is a consequence of reduced responsiveness of paraventricular neurons, but inhibition by opioids or intracerebral oxytocin does not appear to be involved.

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Section: Basal and Stress-induced Activity Of The Hpa Axis In Pregnansupporting

confidence: 70%

Neuroendocrine Responses to Stress in Mice: Hyporesponsiveness in Pregnancy and Parturition

Brunton²,

et al. 2003

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“…Increased production of glucocorticoids during maternal stress mediating embryo-fetal toxicities including cleft palate and skeletal malformations has been proposed as a possible mechanism [4][5][6]21], and has been demonstrated that excess exposure to glucocorticoids retards fetal growth in animals and humans [22,25,30,34]. Subsequent studies proposed placental 11b-hydroxysteroid dehydrogenase, which converts active cortisol to inactive cortisone, as the mechanism guarding fetuses from growth-retarding effects of maternal glucocorticoids [7,35].…”

Section: Introductionmentioning

confidence: 99%

Effect of Maternal Restraint Stress on Fetal Development of ICR Mice

et al. 2008

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“…Visualisation of Crh mRNA expression using an 35 S-labelled probe showed reductions in the density of the autoradiographic signal in the PVN of pregnant and lactating animals compared to dioestrous controls ( Figure 1B). The signal appeared to be partially restored in lactating animals that had been without pups, and thus the suckling stimulus, for 24 hours ( Figure 1B).…”

Section: Crh Mrna Expression Is Suppressed In Pregnant and Lactatinmentioning

confidence: 99%

“…It is possible that the reported corticosterone response to stress in lactating mice by Douglas et al 9 is mediated by increased adrenal cortex sensitivity to circulating ACTH. 35 One mechanism by which ACTH secretion could be regulated in lactation, when Crh mRNA is suppressed, is through an enhanced contribution of AVP to the stress-induced stimulation of ACTH secretion. In the rat, Avp mRNA expression in the PVN is significantly increased during lactation and is proposed to be a major stimulus for ACTH secretion.…”

Section: Endogenous Prolactin Is Not Required For the Maintenance Omentioning

confidence: 99%

The role of prolactin in the suppression of Crh mRNA expression during pregnancy and lactation in the mouse

Gustafson

Bunn

Grattan

2017

J Neuroendocrinology

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Maternal stress is associated with negative health consequences for both the mother and her offspring. To prevent these adverse outcomes, activity of the hypothalamic-pituitary-adrenal (HPA) axis is attenuated during pregnancy and lactation. Although the mechanisms generating this adaptive change have not been defined fully, the anterior pituitary hormone prolactin may play a significant role. The present study investigated the role of prolactin in regulating the basal activity of the HPA axis during pregnancy and lactation in the mouse, focussing upon the corticotrophin-releasing hormone (CRH) neurones. Using in situ hybridisation, a decrease in Crh mRNA-expressing cell number in pregnant (55.6±9.0 cells per section) and lactating (97.4±4.9) mice compared to virgin controls was characterised (186.8±18.7, P<.01 Tukey-Kramer test; n=6-7 per group). Removal of the pups (24 hours) and thus the associated suckling-induced prolactin secretion, restored CRH neurone number (180.1±19.7). To specifically test the role of prolactin in suppressing Crh mRNA expression in lactation, prolactin levels were selectively manipulated in lactating mice. Lactating mice were treated with ovine prolactin (1500 μg day , osmotic minipump, s.c.; n=7) or vehicle (n=6) for 24 hours following pup removal. This was sufficient to suppress Crh mRNA expression from 108.0±13.5 to 53.7±16.7 cells per section (P<.05 Student's t-test). Additional cohorts of lactating mice were treated with bromocriptine (300 μg over 24 hours, s.c.; n=7) or vehicle (n=5) to suppress endogenous prolactin secretion; however, no change in Crh mRNA expression was detected. Thus, although prolactin was sufficient to suppress Crh mRNA expression in the paraventricular nucleus, it does not appear to be required for the ongoing regulation of the CRH neurones in lactation.

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Effects of stress and adrenocorticotrophin administration on plasma corticosterone levels at different stages of pregnancy in the mouse

Cited by 11 publications

References 6 publications

Neuroendocrine Responses to Stress in Mice: Hyporesponsiveness in Pregnancy and Parturition

Neuroendocrine Responses to Stress in Mice: Hyporesponsiveness in Pregnancy and Parturition

Effect of Maternal Restraint Stress on Fetal Development of ICR Mice

The role of prolactin in the suppression of Crh mRNA expression during pregnancy and lactation in the mouse

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