Research reportAdministration of tryptophan-enriched diets to pregnant rats retards the development of the serotonergic system in their offspring
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Perinatal selective serotonin reuptake inhibitor (SSRI) and other antidepressant exposure effects on anxiety and depressive behaviors in offspring: A review of findings in humans and rodent models
2021, Reproductive ToxicologyCitation Excerpt :5-HT is implicated in the pathophysiology of numerous psychiatric and developmental disorders [15–17] and is a target of numerous pharmacological therapies. Long before 5-HT becomes a neurotransmitter in the mature brain, it plays a role as a neurodevelopmental signal and regulates cell growth [8,18,19]. In the fetal brain, 5-HT and its receptors are over-expressed and widespread in regions where they are absent in adults [14,20] pointing to a time-dependent specificity to 5-HT expression during development.
Transfer of maternal psychosocial stress to the fetus
2020, Neuroscience and Biobehavioral ReviewsCitation Excerpt :However, the impact of excessive maternal serotonin concentrations on fetal development is less clear. Feeding of a tryptophan-enriched diet to pregnant rats resulted in hyperserotonaemia (Castrogiovanni et al., 2014; Musumeci et al., 2014), low growth hormone concentration (Musumeci et al., 2014), changes in the expression of 5-HT-regulating genes (Blažević and Hranilović, 2013) and a delayed maturation of the central serotonergic system (Huether et al., 1992) in the developing offspring. Repeated maternal injections of tryptophan administered to pregnant rats resulted in an increased brain serotonin synthesis (Hernandez-Rodriguez and Chagoya, 1986) and reduced anxiety-like behaviour in the offspring (Blazevic et al., 2012).
Extreme enhancement or depletion of serotonin transporter function and serotonin availability in autism spectrum disorder
2019, Pharmacological ResearchCitation Excerpt :Within the placenta TRP is converted to 5-HT by placental TPH1 in early pregnancy (prior to GD 15.5) or transported to the fetal brain in later pregnancy (GD 16.5 to birth) when fetal THP2 is capable of converting TRP to 5-HT to supply fetal 5-HT requirements [40,215]. Either reducing or enhancing TRP availability prenatally or early postnatally in rodent models produces changes in 5-HT synthesis, metabolism, and transport that culminate into respectively worsened or improved adult behavioral phenotypes related to anxiety and depression [225–227]. Disruptions in fetal TRP availability could result not only from TRP deficiency in the maternal diet, but also from increased maternal TRP demand if 5-HT recycling is impaired (e.g., from maternal genetic or pharmacologic reductions in SERT function).
Nutrition
2019, The Laboratory RatOntogeny of monoamine neurotransmitters
2018, Handbook of Developmental NeurotoxicologyCellular resilience: 5-HT neurons in Tph2<sup>-/-</sup> mice retain normal firing behavior despite the lack of brain 5-HT
2015, European NeuropsychopharmacologyCitation Excerpt :Regulation of 5-HT system function by endogenous 5-HT has been implicated in development as well as in the mature brain. Early studies suggested that during embryonic development, released 5-HT, by direct action on autoreceptors (Branchereau et al., 2002; Huether et al., 1992;Whitaker-Azmitia and Azmitia, 1986) and possibly indirectly, via astroglial cells (Whitaker-Azmitia and Azmitia, 1989) causes an auto-inhibitory effect on the serotonergic neuronal phenotype. Later studies revealed an opposite, trophic developmental role of endogenous 5-HT in which 5-HT/5-HT1A receptors together with brain-derived neurotrophic factor (BDNF)/TrkB receptors constitute an autocrine loop that promotes and maintains differentiation of 5-HT neurons (Eaton et al., 1995; Galter and Unsicker, 2000; Rumajogee et al., 2004).