Trick or treat? Evaluating contributing factors and sex-differences for developmental effects of maternal depression and its treatment

Kott, Jennifer; Brummelte, Susanne

doi:10.1016/j.yhbeh.2019.01.004

Cited by 14 publications

(10 citation statements)

References 151 publications

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“…Biological sex is known to interact with the prenatal environment through a number of sex‐specific mechanisms, which may impact both the extent and effect of early adverse exposures (DiPietro & Voegtline, 2017). In animal models, developmental SSRI exposure has been associated with a number of sexually differentiated brain and behavioral outcomes (Kott & Brummelte, 2019). For example, male rats pups with perinatal citalopram exposure were more severely compromised than females, exhibiting disrupted behavior and a greater percentage of abnormal axons (Simpson et al., 2011), while perinatal fluoxetine increased depressive‐like behaviors in adolescent female (Lisboa et al., 2007) and anxiety‐like behaviors in adult male rodents (Gobinath et al., 2016).…”

Section: Introductionmentioning

confidence: 99%

Prenatal antidepressant exposure and sex differences in neonatal corpus callosum microstructure

Campbell

Williams

Björnson

et al. 2021

Developmental Psychobiology

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Prenatal exposure to selective serotonin reuptake inhibitor (SSRI) antidepressants may influence white matter (WM) development, as previous studies report widespread microstructural alterations and reduced interhemispheric connectivity in SSRI‐exposed infants. In rodents, perinatal SSRIs had sex‐specific disruptions in corpus callosum (CC) axon architecture and connectivity; yet it is unknown whether SSRI‐related brain outcomes in humans are sex specific. In this study, the neonate CC was selected as a region‐of‐interest to investigate whether prenatal SSRI exposure has sex‐specific effects on early WM microstructure. On postnatal day 7, diffusion tensor imaging was used to assess WM microstructure in SSRI‐exposed (n = 24; 12 male) and nonexposed (n = 48; 28 male) term‐born neonates. Fractional anisotropy was extracted from CC voxels and a multivariate discriminant analysis was used to identify latent patterns differing between neonates grouped by SSRI‐exposure and sex. Analysis revealed localized variations in CC fractional anisotropy that significantly discriminated neonate groups and correctly predicted group membership with an 82% accuracy. Such effects were identified across three dimensions, representing sex differences in SSRI‐exposed neonates (genu, splenium), SSRI‐related effects independent of sex (genu‐to‐rostral body), and sex differences in nonexposed neonates (isthmus‐splenium, posterior midbody). Our findings suggest that CC microstructure may have a sex‐specific, localized, developmental sensitivity to prenatal SSRI exposure.

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Section: Introductionmentioning

confidence: 99%

Prenatal antidepressant exposure and sex differences in neonatal corpus callosum microstructure

Campbell

Williams

Björnson

et al. 2021

Developmental Psychobiology

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“…In the United States, it is estimated that greater than 50% of women are diagnosed as overweight or obese at their first prenatal visit 5 . High maternal weight creates an environment of chronic inflammation and is associated with numerous negative outcomes, both maternal and fetal [1][2][3][4] . Despite this, mechanisms through which chronic maternal inflammation driven by high maternal weight impact offspring neurodevelopment are scarce.…”

Section: Discussionmentioning

confidence: 99%

“…

High maternal weight is associated with a number of detrimental outcomes in offspring, including increased susceptibility to neurological disorders such as anxiety, depression, and communicative disorders (e.g. autism spectrum disorders) [1][2][3][4][5][6][7][8] . Despite widespread acknowledgement of sex-biases in the prevalence, incidence, and age of onset of these disorders, few studies have investigated potential sex-biased mechanisms underlying disorder susceptibility.

…”

mentioning

confidence: 99%

Maternal diet disrupts the placenta-brain axis in a sex-specific manner

Ceasrine

Devlin

Bolton

et al. 2021

Preprint

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SUMMARYHigh maternal weight is associated with a number of detrimental outcomes in offspring, including increased susceptibility to neurological disorders such as anxiety, depression, and communicative disorders (e.g. autism spectrum disorders)1–4. Despite widespread acknowledgement of sex-biases in the prevalence, incidence, and age of onset of these disorders, few studies have investigated potential sex-biased mechanisms underlying disorder susceptibility. Here, we use a mouse model to demonstrate how maternal high-fat diet causes perinatal inflammation that influences sex-specific behavioral outcomes in offspring. In male high-fat diet offspring, increased macrophage toll like receptor 4 signaling results in excess phagocytosis of serotonin neurons in the developing dorsal raphe nucleus, decreasing serotonin bioavailability in the fetal and adult brain. Bulk sequencing from a large cohort of matched first trimester human fetal brain, placenta, and maternal decidua samples reveals sex-specific transcriptome-wide changes in placenta and brain tissue. Further, we find that fetal brain serotonin is significantly negatively correlated with maternal triglyceride accumulation (a proxy for dietary fat content) in male pregnancies only. These findings uncover a fundamental mechanism through which maternal diet may increase offspring susceptibility for neuropsychiatric disorder development.

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“…Due to inconsistent study results, review outcomes differ. There is a tendency, however, towards viewing SSRI exposure as a plasticity rather than a risk factor [167][168][169][170][171][172][173]. This means that SSRI exposure can positively or negatively influence offspring's 5-HT system depending on other gestational factors.…”

Section: Maternal Intake Of 5-ht-ergic Medication Alters 5-ht Levels mentioning

confidence: 99%

Gestational Factors throughout Fetal Neurodevelopment: The Serotonin Link

Hanswijk

Spoelder

Shan

et al. 2020

IJMS

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Serotonin (5-HT) is a critical player in brain development and neuropsychiatric disorders. Fetal 5-HT levels can be influenced by several gestational factors, such as maternal genotype, diet, stress, medication, and immune activation. In this review, addressing both human and animal studies, we discuss how these gestational factors affect placental and fetal brain 5-HT levels, leading to changes in brain structure and function and behavior. We conclude that gestational factors are able to interact and thereby amplify or counteract each other’s impact on the fetal 5-HT-ergic system. We, therefore, argue that beyond the understanding of how single gestational factors affect 5-HT-ergic brain development and behavior in offspring, it is critical to elucidate the consequences of interacting factors. Moreover, we describe how each gestational factor is able to alter the 5-HT-ergic influence on the thalamocortical- and prefrontal-limbic circuitry and the hypothalamo-pituitary-adrenocortical-axis. These alterations have been associated with risks to develop attention deficit hyperactivity disorder, autism spectrum disorders, depression, and/or anxiety. Consequently, the manipulation of gestational factors may be used to combat pregnancy-related risks for neuropsychiatric disorders.

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Trick or treat? Evaluating contributing factors and sex-differences for developmental effects of maternal depression and its treatment

Cited by 14 publications

References 151 publications

Prenatal antidepressant exposure and sex differences in neonatal corpus callosum microstructure

Prenatal antidepressant exposure and sex differences in neonatal corpus callosum microstructure

Maternal diet disrupts the placenta-brain axis in a sex-specific manner

Gestational Factors throughout Fetal Neurodevelopment: The Serotonin Link

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