Prenatal SSRI exposure alters neonatal corticosteroid binding globulin, infant cortisol levels, and emerging HPA function

Pawluski, Jodi L.; Brain, Ursula; Underhill, Caroline; Hammond, Geoffrey L.; Oberlander, Tim F.

doi:10.1016/j.psyneuen.2011.11.011

Cited by 73 publications

(51 citation statements)

References 41 publications

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“…This indicates that PRS was effective in inducing the hyper-responsiveness of the HPA axis, as shown by previous studies, which have demonstrated that early life experiences, including maternal stress, are linked to anxiety and depressed behavior in adolescence and adulthood, in parallel with hyperactivity of the HPA axis [9][10][11][12][13].…”

Section: Discussionsupporting

confidence: 78%

“…Several clinical and preclinical studies have shown that exposure to maternal mood disorders, maternal stress and other forms of maternal hardship can affect the developing hypothalamic-pituitary-adrenal (HPA) axis [4][5][6][7][8]. Many studies have demonstrated that early life experiences, including maternal stress, are linked to anxiety and depressed behavior in adolescence and adulthood, in parallel with hyperactivity of the HPA axis [9][10][11][12][13].…”

Section: Introductionmentioning

confidence: 99%

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Prenatal Restraint Stress is Associated with Demethylation of Corticotrophin Releasing Hormone (CRH) Promoter and Enhances CRH Transcriptional Responses to Stress in Adolescent Rats

Sun

Gao

et al. 2014

Neurochem Res

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Maternal stress can disturb normal fetal neurodevelopmental progress, and lead to negative behavioral and neuroendocrine consequences for the offspring. These effects may be related to alterations in the hypothalamic-pituitary-adrenal (HPA) axis. Early life events disrupting the function of the HPA axis may be associated with epigenetic modification. This study investigated the effect of maternal stress on the methylation rate of the corticotrophin-releasing hormone (CRH) promoter and HPA axis response to acute stress in the adolescent offspring of Sprague-Dawley rats. Pregnant dams were randomly assigned to two groups: restraint stress group and normal control group. Adolescent male and female offspring were used from each group. The results showed that prenatal stress is associated with the demethylation of the CRH promoter, and leads to anxiety-like behaviors in adolescent life stages, as well as hyper-responsiveness of the HPA axis. Together, these results imply that prenatal stress alters the normal HPA function, which may be via the epigenetic mechanism.

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Section: Discussionsupporting

confidence: 78%

Section: Introductionmentioning

confidence: 99%

Prenatal Restraint Stress is Associated with Demethylation of Corticotrophin Releasing Hormone (CRH) Promoter and Enhances CRH Transcriptional Responses to Stress in Adolescent Rats

Sun

Gao

et al. 2014

Neurochem Res

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“…30% in the current study), resulting in relaxation of the anal sphincter and meconium excretion, as well a low Apgar score at 1 min [1,7]. We speculate that the hypothalmic-pituitary-adrenal axis of fetuses exposed to SRI medications may be depressed [16] and that their ability to tolerate stressogenic events is lowered. We should stress that no cases of meconium aspiration syndrome were documented.…”

Section: Discussionmentioning

confidence: 94%

Short-Term Neonatal Outcome among Term Infants after in utero Exposure to Serotonin Reuptake Inhibitors

Leibovitch¹,

Rymer-Haskel²,

Schushan-Eisen³

et al. 2013

Neonatology

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Background: Serotonin reuptake inhibitor (SRI) medications are commonly in use during pregnancy. Objectives: To evaluate short-term neonatal clinical signs among infants exposed to intrauterine SRI medications, in order to estimate the need for postnatal monitoring and observation. Methods: Retrospective review of clinical data in medical files of term infants born to mothers who reported treatment with SRIs during pregnancy. Results: Out of 401 infants in the study group, 165 (41%) were reported to have at least 1 clinical symptom, including respiratory distress, jitteriness, restlessness, feeding difficulties, regurgitations, fever ≥38°C, a short cyanotic event and convulsions. In the symptomatic group, 70% exhibited mild symptoms, among them restlessness, jitteriness or feeding difficulties, while around 30% exhibited significant symptoms. Overall, 12% of the total cohort, mostly males (70%), presented significant clinical symptoms, but none had an urgent or life-threatening condition. Infants in the study group were shorter in length and had a higher rate of Apgar score <7 at 1 min, meconium-stained amniotic fluid and respiratory distress. Conclusions: Despite the high incidence of clinical signs among infants born to SRI-treated mothers, most of their symptoms were mild and self-limited. These infants should be observed while they are close to their mothers on the maternity ward for 48 h after birth.

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“…In early infancy in utero SRI exposure affects cortisol levels and its binding protein, corticosteroid-binding globulin (CBG) (Pawluski, Brain, Underhill, Hammond, & Oberlander, 2011 ). Exposed neonates had increased CBG levels, particularly after vaginal delivery, though cord cortisol levels did not vary with in utero SRI exposure or antenatal maternal mood.…”

Section: Stress Regulationmentioning

confidence: 99%

“…At 3 months, SRI exposed infants had a reduced diurnal change in salivary cortisol, possibly suggesting that prenatal SRI exposure affects the developing HPA system via altered serum neonatal CBG levels (Pawluski et al, 2011 ). This also may be refl ected in altered HPA stress patterns and lower early evening basal cortisol levels in SRI exposed infants .…”

Section: Stress Regulationmentioning

confidence: 99%

Fetal Effects of In Utero Serotonin Reuptake Inhibitor (SRI) Antidepressant Exposure

et al. 2016

Self Cite

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In utero serotonin reuptake inhibitor (SRI) exposure is relatively common and neonatal behavioral outcomes vary greatly. Such exposure has led to questions about whether these effects refl ect an acute short-lived pharmacological phenomenon that results in a "withdrawal" condition, or sustained neurological changes associated with altered serotonin (5-HT) signaling that begins long before birth. Emerging reports now suggest that certain effects associated with in utero SRI exposure become evident during gestation. For instance, in utero SRI exposure appears to infl uence fetal brain blood fl ow and neurobehavior. In this chapter, we summarize current research evidence reporting the fetal effects of in utero SRI exposure. Given the paucity of empiric fetal data in humans, we draw from what we know about three postnatal fi ndings that may refl ect fetal developmental sequelae associated with in utero SRI exposure.

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Prenatal SSRI exposure alters neonatal corticosteroid binding globulin, infant cortisol levels, and emerging HPA function

Cited by 73 publications

References 41 publications

Prenatal Restraint Stress is Associated with Demethylation of Corticotrophin Releasing Hormone (CRH) Promoter and Enhances CRH Transcriptional Responses to Stress in Adolescent Rats

Prenatal Restraint Stress is Associated with Demethylation of Corticotrophin Releasing Hormone (CRH) Promoter and Enhances CRH Transcriptional Responses to Stress in Adolescent Rats

Short-Term Neonatal Outcome among Term Infants after in utero Exposure to Serotonin Reuptake Inhibitors

Fetal Effects of In Utero Serotonin Reuptake Inhibitor (SRI) Antidepressant Exposure

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