Perinatal Selective Serotonin Reuptake Inhibitor Exposure: Impact on Brain Development and Neural Plasticity

Pawluski, Jodi L.

doi:10.1159/000329293

Cited by 25 publications

(20 citation statements)

References 107 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: 77%

“…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: 77%

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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“…Moreover epigenetic modifications may contribute to developmental outcomes (Kinnally et al, 2010). Overall, early exposure to SSRIs has an effect on brain development and neuroplasticity (for review see: Pawluski, 2012) which can markedly alter the behavior of the offspring.…”

Section: Selective Serotonin Reuptake Inhibitorsmentioning

confidence: 99%

The effects of maternal depression and maternal selective serotonin reuptake inhibitor exposure on offspring

Olivier¹,

Åkerud²,

Kaihola³

et al. 2013

Front. Cell. Neurosci.

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It has been estimated that 20% of pregnant women suffer from depression and it is well-documented that maternal depression can have long-lasting effects on the child. Currently, common treatment for maternal depression has been the selective serotonin reuptake inhibitor medications (SSRIs) which are used by 2–3% of pregnant women in the Nordic countries and by up to 10% of pregnant women in the United States. Antidepressants cross the placenta and are transferred to the fetus, thus, the question arises as to whether children of women taking antidepressants are at risk for altered neurodevelopmental outcomes and, if so, whether the risks are due to SSRI medication exposure or to the underlying maternal depression. This review considers the effects of maternal depression and SSRI exposure on offspring development in both clinical and preclinical populations. As it is impossible in humans to study the effects of SSRIs without taking into account the possible underlying effects of maternal depression (healthy pregnant women do not take SSRIs), animal models are of great value. For example, rodents can be used to determine the effects of maternal depression and/or perinatal SSRI exposure on offspring outcomes. Unraveling the joint (or separate) effects of maternal depression and SSRI exposure will provide more insights into the risks or benefits of SSRI exposure during gestation and will help women make informed decisions about using SSRIs during pregnancy.

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“…It should be emphasized that we examined healthy animals that were not subjected to conditions simulating maternal depression or stress. Maternal stress, which has been shown to influence the actions of developmental SSRI exposure using murine models [46], was therefore not accounted for in the present study design.…”

Section: Discussionmentioning

confidence: 99%

Developmental Exposure to Fluoxetine Modulates the Serotonin System in Hypothalamus

Berg

Bäckström²,

Winberg³

et al. 2013

PLoS ONE

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The selective serotonin reuptake inhibitor (SSRI) fluoxetine (FLU, Prozac®) is commonly prescribed for depression in pregnant women. This results in SSRI exposure of the developing fetus. However, there are knowledge gaps regarding the impact of SSRI exposure during development. Given the role of serotonin in brain development and its cross-talk with sex hormone function, we investigated effects of developmental exposure to pharmacologically relevant concentrations of FLU (3 and 30 nM (measured)) on brain neurotransmitter levels, gonadal differentiation, aromatase activity in brain and gonads, and the thyroid system, using the Xenopus tropicalis model. Tadpoles were chronically exposed (8 weeks) until metamorphosis. At metamorphosis brains were cryosectioned and levels of serotonin, dopamine, norepinephrine, and their metabolites 5-hydroxyindoleacetic acid, 3,4-dihydroxyphenylacetic acid, and homovanillic acid were measured in discrete regions (telencephalon, hypothalamus and the reticular formation) of the cryosections using high-performance liquid chromatography. Exposure to 30 nM FLU increased the concentration of 5-hydroxyindoleacetic acid in hypothalamus compared with controls. FLU exposure did not affect survival, time to metamorphosis, thyroid histology, gonadal sex differentiation, or aromatase activity implying that the effect on the serotonergic neurotransmitter system in the hypothalamus region was specific. The FLU concentration that impacted the serotonin system is lower than the concentration measured in umbilical cord serum, suggesting that the serotonin system of the developing brain is highly sensitive to in utero exposure to FLU. To our knowledge this is the first study showing effects of developmental FLU exposure on brain neurochemistry. Given that SSRIs are present in the aquatic environment the current results warrant further investigation into the neurobehavioral effects of SSRIs in aquatic wildlife.

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Perinatal Selective Serotonin Reuptake Inhibitor Exposure: Impact on Brain Development and Neural Plasticity

Cited by 25 publications

References 107 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

The effects of maternal depression and maternal selective serotonin reuptake inhibitor exposure on offspring

Developmental Exposure to Fluoxetine Modulates the Serotonin System in Hypothalamus

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