Fluoxetine during Development Reverses the Effects of Prenatal Stress on Depressive-Like Behavior and Hippocampal Neurogenesis in Adolescence

Rayen, Ine; Hove, Daniël L.A. van den; Prickaerts, Jos; Steinbusch, Harry W.M.; Pawluski, Jodi L.

doi:10.1371/journal.pone.0024003

Cited by 155 publications

(193 citation statements)

References 71 publications

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“…Emerging reports from animal models suggest that early SRI exposure has a positive influence, reversing or "correcting" the adverse effects of prenatal maternal stress exposure (32)(33)(34). Although they are of interest, our results are not entirely consistent with that pattern, as, in our case, SRI exposure appears to lead to an "over-correction."…”

Section: Discussioncontrasting

confidence: 77%

Prenatal exposure to antidepressants and depressed maternal mood alter trajectory of infant speech perception

Weikum

Oberlander

Hensch

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

168

102

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Language acquisition reflects a complex interplay between biology and early experience. Psychotropic medication exposure has been shown to alter neural plasticity and shift sensitive periods in perceptual development. Notably, serotonin reuptake inhibitors (SRIs) are antidepressant agents increasingly prescribed to manage antenatal mood disorders, and depressed maternal mood per se during pregnancy impacts infant behavior, also raising concerns about long-term consequences following such developmental exposure. We studied whether infants' language development is altered by prenatal exposure to SRIs and whether such effects differ from exposure to maternal mood disturbances. Infants from non-SRI-treated mothers with little or no depression (control), depressed but non-SRI-treated (depressed-only), and depressed and treated with an SRI (SRI-exposed) were studied at 36 wk gestation (while still in utero) on a consonant and vowel discrimination task and at 6 and 10 mo of age on a nonnative speech and visual language discrimination task. Whereas the control infants responded as expected (success at 6 mo and failure at 10 mo) the SRI-exposed infants failed to discriminate the language differences at either age and the depressed-only infants succeeded at 10 mo instead of 6 mo. Fetuses at 36 wk gestation in the control condition performed as expected, with a response on vowel but not consonant discrimination, whereas the SRI-exposed fetuses showed accelerated perceptual development by discriminating both vowels and consonants. Thus, prenatal depressed maternal mood and SRI exposure were found to shift developmental milestones bidirectionally on infant speech perception tasks.L anguage, our most quintessential human characteristic, involves a complex interplay between biology and experience. At birth, infants possess an initial preparedness for language and a developmental readiness that supports learning any of the world's languages (1-3), yet also already show privileged processing to the native language from prenatal listening experience (4-6). During the following weeks and months of life, infants become progressively attuned to the properties of their native language, including its rhythmical and segmental (e.g., consonant) information (reviewed in refs. 7 and 8). The high degree of regularity in the timing of sequential tuning to properties of the native language suggests a series of critical or sensitive periods, i.e., points in development when the system is maximally influenced by input.The timing of onset of these sensitive periods seems to be maturationally constrained. Infants born 3 mo preterm attune to the phonetic properties (9) of their native language at the same gestational age as full-term infants, not according to the number of months of postnatal listening experience. Such maturational constraints can protect development: ensuring the optimal consecutive stabilization of the perceptual components that contribute in a step-wise fashion to language acquisition (10). However, it is known from research i...

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Section: Discussioncontrasting

confidence: 77%

Prenatal exposure to antidepressants and depressed maternal mood alter trajectory of infant speech perception

Weikum

Oberlander

Hensch

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

168

102

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“…Results from animal models of maternal stress support these data and indicate that volumetric abnormalities in prenatally stressed offspring reflect reduced numbers of both neurons and glia, in particular in the hippocampus and amygdala due, in part, to decreased neurogenesis (Coe et al, 2003;Fujioka et al, 2006;Kawamura et al, 2006;Kraszpulski et al, 2006;Lemaire et al, 2000;Rayen et al, 2011). Further, reduced synaptogenesis and hypo-myelination in limbic regions was found in male, but not in female, juvenile rats exposed to maternal stress (Murmu et al, 2006;Xu et al, 2013).…”

Section: Reprogramming In the Prenatally Stressed Brainmentioning

confidence: 62%

The Placenta as a Mediator of Stress Effects on Neurodevelopmental Reprogramming

Bronson

Bale

2015

Neuropsychopharmacol

196

170

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Adversity experienced during gestation is a predictor of lifetime neuropsychiatric disease susceptibility. Specifically, maternal stress during pregnancy predisposes offspring to sex-biased neurodevelopmental disorders, including schizophrenia, attention deficit/hyperactivity disorder, and autism spectrum disorders. Animal models have demonstrated disease-relevant endophenotypes in prenatally stressed offspring and have provided unique insight into potential programmatic mechanisms. The placenta has a critical role in the deleterious and sex-specific effects of maternal stress and other fetal exposures on the developing brain. Stress-induced perturbations of the maternal milieu are conveyed to the embryo via the placenta, the maternal-fetal intermediary responsible for maintaining intrauterine homeostasis. Disruption of vital placental functions can have a significant impact on fetal development, including the brain, outcomes that are largely sex-specific. Here we review the novel involvement of the placenta in the transmission of the maternal adverse environment and effects on the developing brain.

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“…In mice, maternal fluoxetine in early development reversed the effects of prenatal maternal stress on depressive-like behaviors and hippocampal neurogenesis in adolescent offspring. 8 In humans, SSRIs cross the placenta, 9 reduce serotonin reuptake in the placenta 10 and fetus, 11 and may reduce uterine blood flow, leading to fetal hypoxemia. 12 Fetal hypoxia can adversely affect birth and developmental outcomes; an association with ASD is plausible.…”

Section: Discussionmentioning

confidence: 99%

Prenatal SSRI Use and Offspring With Autism Spectrum Disorder or Developmental Delay

et al. 2014

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WHAT'S KNOWN ON THIS SUBJECT: Serotonin is critical in early brain development, creating concerns regarding prenatal exposure to factors influencing serotonin levels, like selective serotonin reuptake inhibitors (SSRIs). Prenatal SSRI use was recently associated with autism; however, its association with other developmental delays is unclear. WHAT THIS STUDY ADDS:This population-based case-control study in young children provides evidence that prenatal SSRI use may be a risk factor for autism and other developmental delays. However, underlying depression and its genetic underpinnings may be a confounder.abstract OBJECTIVE: To examine associations between prenatal use of selective serotonin reuptake inhibitors (SSRIs) and the odds of autism spectrum disorders (ASDs) and other developmental delays (DDs).METHODS: A total of 966 mother-child pairs were evaluated (492 ASD, 154 DD, 320 typical development [TD]) from the Childhood Autism Risks from Genetics and the Environment (CHARGE) Study, a populationbased case-control study. Standardized measures confirmed developmental status. Interviews with biological mothers ascertained prenatal SSRI use, maternal mental health history, and sociodemographic information. RESULTS:Overall, prevalence of prenatal SSRI exposure was lowest in TD children (3.4%) but did not differ significantly from ASD (5.9%) or DD (5.2%) children. Among boys, prenatal SSRI exposure was nearly 3 times as likely in children with ASD relative to TD (adjusted odds ratio [OR]: 2.91; 95% confidence interval [CI]: 1.07-7.93); the strongest association occurred with first-trimester exposure (OR: 3.22; 95% CI: 1.17-8.84). Exposure was also elevated among boys with DD (OR: 3.39; 95% CI: 0.98-11.75) and was strongest in the third trimester (OR: 4.98; 95% CI: 1.20-20.62). Findings were similar among mothers with an anxiety or mood disorder history. CONCLUSIONS:In boys, prenatal exposure to SSRIs may increase susceptibility to ASD or DD. Findings from published studies on SSRIs and ASD continues to be inconsistent. Potential recall bias and residual confounding by indication are concerns. Larger samples are needed to replicate DD results. Because maternal depression itself carries risks for the fetus, the benefits of prenatal SSRI use should be carefully weighed against potential harms.

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Fluoxetine during Development Reverses the Effects of Prenatal Stress on Depressive-Like Behavior and Hippocampal Neurogenesis in Adolescence

Cited by 155 publications

References 71 publications

Prenatal exposure to antidepressants and depressed maternal mood alter trajectory of infant speech perception

Prenatal exposure to antidepressants and depressed maternal mood alter trajectory of infant speech perception

The Placenta as a Mediator of Stress Effects on Neurodevelopmental Reprogramming

Prenatal SSRI Use and Offspring With Autism Spectrum Disorder or Developmental Delay

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