Developmental changes in serotonin signaling: Implications for early brain function, behavior and adaptation

Brummelte, Susanne; Glanaghy, Edel Mc; Bonnin, Alexandre; Oberlander, Tim F.

doi:10.1016/j.neuroscience.2016.02.037

Cited by 218 publications

(182 citation statements)

References 216 publications

(312 reference statements)

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“…It has been suggested that pregnancy conditions such as maternal stress and inflammation up-regulate placental serotonin production to program the developing fetus for neurodevelopmental disorders (St Pierre et al 2015; Goeden et al 2016; Brummelte et al 2016). Increased IL-1 and IL-6 have been identified as potential cytokines linked to changes in placental function and subsequent neurodevelopmental insults that include forebrain damage and behavioral consequences in rodents (Smith et al 2007; Girard et al 2010).…”

Section: Long-term Outcomes Of Children Born To Obese Mothersmentioning

confidence: 99%

Effects of maternal obesity on placental function and fetal development

2017

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Obesity has reached epidemic proportions and pregnancies in obese mothers have increased risk for complications including gestational diabetes, hypertensive disorders, preterm birth and caesarian section. Children born to obese mothers are at increased risk of obesity and metabolic disease and are susceptible to develop neuropsychiatric and cognitive disorders. Changes in placental function not only play a critical role in the development of pregnancy complications but may also be involved in linking maternal obesity to long-term health risks in the infant. Maternal adipokines i.e., interleukin 6 (IL-6), tumor necrosis factor alpha (TNF-α), leptin and adiponectin link maternal nutritional status and adipose tissue metabolism to placental function. Adipokines and metabolic hormones have direct impact on placental function by modulating placental nutrient transport. Nutrient delivery to the fetus is regulated by a complex interaction between insulin signaling, cytokine profile and insulin responsiveness, which is modulated by adiponectin and IL-1β. In addition, obese pregnant women are at risk for hypertension and preeclampsia with reduced placental vascularity and blood flow, which would restrict placental nutrient delivery to the developing fetus. These sometimes opposing signals regulating placental function may contribute to the diversity of short and long-term outcomes observed in pregnant obese women. This review focuses on the changes in adipokines and obesity-related metabolic hormones, how these factors influence placental function and fetal development to contribute to long-term metabolic and behavioral consequences of children born to obese mothers.

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Section: Long-term Outcomes Of Children Born To Obese Mothersmentioning

confidence: 99%

Effects of maternal obesity on placental function and fetal development

2017

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“…Not surprisingly, like in non-mammalian species, serotonin modulates neuronal proliferation, migration and differentiation. In addition, 5-HT is implicated in the emergence of many neuropsychiatric disorders, including mental retardation, autism, depression and anxiety [10,15,[21][22][23][24][25][26]. Importantly, 5-HT signalling is influenced by numerous epigenetic and genetic factors, including nutrition and gut microbiota [27,28], perinatal stress [29][30][31], infection and inflammation [32][33][34][35], 5-HT metabolism and storage [15,[36][37][38], pharmacological compounds such as selective serotonin reuptake inhibitors [38][39][40] and genetic alterations [41][42][43][44].…”

Section: Introductionmentioning

confidence: 99%

Sculpting Cerebral Cortex with Serotonin in Rodent and Primate

Vitalis¹,

Verney²

2017

Serotonin - A Chemical Messenger Between All Types of Living Cells

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The mammalian cerebral cortex is critical for sensory and motor integrations and, for higher-order cognitive functions. The construction of mammalian cortical circuits involves the coordinated interplay between cellular processes such as proliferation, migration and differentiation of neural and glial cell subtypes followed by accurate connectivity evolving in complexity in primates. Alteration in cortical development may induce the emergence of various pathological traits and behaviours. Among the large array of factors that regulate the assembly of cortical circuits, serotonin (5-HT) plays important role as a developmental signal that impacts on a broad diversity of cellular processes. 5-HT plays distinct roles during specific sensitive periods and is produced from various sources depending on the perinatal stage. Its roles are mediated by more than fourteen 5-HT receptors that are all G-protein coupled receptors except the ionotropic 5-HT type 3A receptor (5-HT 3A ) mediating rapid neuronal activation. Importantly, 5-HT metabolism and signalling are influenced by numerous epigenetic and genetic factors, including nutrition and gut microbiota, perinatal stress, infection and inflammation. In this review, we will recapitulate some evidences showing that dysregulation of 5-HT homeostasis and 5-HT 3A signalling impairs distinct steps of cortical circuit formation leading to the predisposition of the onset of various psychiatric diseases.

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“…Selective serotonin reuptake inhibition (5HT), caused by the use of fluoxetine, increases the extracellular concentration of this neurotransmitter, which plays important roles in the regulation of behavior, mood, anxiety, aggressiveness, depression, sleep, fatigue and appetite suppression 6 .…”

Section: Introductionmentioning

confidence: 99%

Fluoxetine effects on periodontogenesis: histomorphometrical and immunohistochemical analyses in rats

et al. 2017

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Reports have indicated that serotonin plays an important role in cell migration and differentiation during the organogenesis of several tissues, including the oral types. Administration of selective serotonin reuptake inhibitor (SSRI) drugs during pregnancy could affect the delivery of serotonin to embryonic tissues altering its development. Objective This study aimed to assess the effects of fluoxetine, a selective serotonin reuptake inhibitor, on the formation of the periodontal ligament during pregnancy and lactation in rat pups.Material and Methods Twelve pregnant rats of Wistar lineage were divided into four study groups. In the control group, 0.9% sodium chloride solution was administered orally, throughout the entire period of the 21 days of pregnancy (CG group) and in the CGL group, it was administrated during pregnancy and lactation (from day 1 of pregnancy to the 21st day after birth). Fluoxetine was administered orally at the dose of 20 mg/kg in a group treated during pregnancy only (FG group), and during pregnancy and lactation (FGL group). Histometrical, histochemical and immunohistochemical analysis of the maxillary first molar periodontium region of the 24 rat pups was made under light microscopy, and periodontal ligament collagen was qualitatively evaluated under a polarizing light microscope.Results The quantity of fibroblasts (p=0.006), osteoblasts (p=0.027) and cementoblasts (p=0.001) was reduced in pups from the rats that received fluoxetine during pregnancy and lactation. No alterations were seen in the collagen fibers.Conclusion These findings suggest that periodontal tissue may be sensitive to fluoxetine, and its interference in reducing periodontal cells depends on exposure time during lactation.

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Developmental changes in serotonin signaling: Implications for early brain function, behavior and adaptation

Cited by 218 publications

References 216 publications

Effects of maternal obesity on placental function and fetal development

Effects of maternal obesity on placental function and fetal development

Sculpting Cerebral Cortex with Serotonin in Rodent and Primate

Fluoxetine effects on periodontogenesis: histomorphometrical and immunohistochemical analyses in rats

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