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Gestational Factors Throughout Fetal Neurodevelopment: the Serotonin Link

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Gestational Factors Throughout Fetal Neurodevelopment: the Serotonin Link International Journal of Molecular Sciences Review Gestational Factors throughout Fetal Neurodevelopment: The Serotonin Link Sabrina I. Hanswijk 1 , Marcia Spoelder 1, Ling Shan 2 , Michel M. M. Verheij 1, 1 3 3 4, Otto G. Muilwijk , Weizhuo Li , Chunqing Liu , Sharon M. Kolk y and 1, , Judith R. Homberg * y 1 Department of Cognitive Neuroscience, Donders Institute for Brain, Cognition and Behavior, Radboud University Nijmegen Medical Centre, 6525 EN Nijmegen, The Netherlands; [email protected] (S.I.H.); [email protected] (M.S.); [email protected] (M.M.M.V.); [email protected] (O.G.M.) 2 Netherlands Institute for Neuroscience, an Institute of the Royal Netherlands Academy of Arts and Sciences, 1105 BA Amsterdam, The Netherlands; [email protected] 3 College of Medical Laboratory, Dalian Medical University, Dalian 116044, China; [email protected] (W.L.); [email protected] (C.L.) 4 Department of Molecular Neurobiology, Donders Institute for Brain, Cognition and Behavior, Radboud University, 6525 AJ Nijmegen, The Netherlands; [email protected] * Correspondence: [email protected]; Tel.: + 31-24-3610906 These authors contributed equally to this work. y Received: 23 June 2020; Accepted: 11 August 2020; Published: 14 August 2020 Abstract: 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. Keywords: gestation; serotonin; neurodevelopment; neural circuit formation; neuropsychiatric disorders 1. Introduction The neurotransmitter serotonin (5-HT) plays a major role in neuropsychiatric disorders and is a key player in brain development [1,2]. In adulthood, 5-HT cannot cross the blood–brain barrier, while its precursors tryptophan and 5-hydroxytryptophan (5-HTP) can (see review [3]). However, roughly during the first half of pregnancy, 5-HT can be transferred from the mother’s placenta, via the fetal periphery, to the fetal brain [4–6]. It is, therefore, likely that the maternal environment can greatly influence fetal brain development. This, in turn, may play a role in the onset of multiple neuropsychiatric disorders, as many of these disorders seem to have a developmental origin [7]. Further insight into how gestational factors can influence the fetal 5-HT system may advance our understanding of the aetiology underlying several neuropsychiatric disorders. Int. J. Mol. Sci. 2020, 21, 5850; doi:10.3390/ijms21165850 www.mdpi.com/journal/ijms Int. J. Mol. Sci. 2020, 21, x FOR PEER REVIEW 2 of 42 1.1. The 5-HT System and Its Embryonic Development As illustrated in Figure 1, 5-HT signaling is tightly controlled by (1) tryptophan hydroxylase (TPH), the rate-limiting enzyme of 5-HT synthesis, and by (2) the 5-HT transporter (5-HTT), which is responsible for the high-affinity reuptake of 5-HT. Two TPH isoforms have been identified to synthesize 5-HT from tryptophan. TPH1 is responsible for 5-HT synthesis in the periphery and to a smaller extent also in the brain pineal gland. TPH2 is essential for 5-HT synthesis in the brain [8,9]. In addition, TPH2 is also important for 5-HT synthesis in the enteric nervous system and thereby the regulation of gastrointestinal motility [10]. In the brain, 5-HT is synthesized by 5-HT-ergic neurons located in the various nuclei of the raphe nuclei in the brainstem and is transported into synaptic Int. J.vesicles Mol. Sci. 2020by the, 21 ,vesicular 5850 monoamine transporter isoform 2. The exocytosis of these vesicles releases2 of 41 5-HT into the synaptic cleft, where it binds to post-synaptic 5-HT receptors. Thus far, at least 14 different 5-HT receptor subtypes have been identified (5-HT1A/B/D/E/F, 5-HT2A/B/C, 5-HT3, 5-HT4, 5-HT5A/B, 1.1. The5-HT 5-HT6, and System 5-HT7), and which ItsEmbryonic can trigger Development a variety of signaling cascades. All but the 5-HT3 receptor are metobotropic and belong to the G protein-coupled receptor superfamily. A complete overview of the receptor’sAs illustrated transduction in Figure mechanisms1, 5-HT signaling is beyond is tightly the scope controlled of this by review (1) tryptophan and has been hydroxylase discussed (TPH),in the rate-limitingdetail previously enzyme [11,12]. of 5-HT Of note, synthesis, at the andcost byof (2)5-HT, the tryptophan 5-HT transporter can also (5-HTT), serve as which a precursor is responsible of for thekynurenine high-affinity via the reuptake rate-limiting of 5-HT. enzymes Two TPH tryptoph isoformsan 2,3-dioxygenase have been identified (TDO) and to synthesize indoleamine 5-HT 2,3- from tryptophan.dioxygenase TPH1 (IDO) is responsible [13]. Kynurenine for 5-HT is synthesisfurther degraded in the periphery into multiple and to neuroactive a smaller extentmetabolites, also in the brainincluding pineal gland. kynurenic TPH2 acid is essentialand quinolinic for 5-HT acid. synthesis The kynurenine in the brain pathway [8,9 ].plays In addition, a role in TPH2immune is also importantresponse for and 5-HT inflammation synthesis in [14,15]. the enteric nervous system and thereby the regulation of gastrointestinal motility [The10]. various In the brain,developmental 5-HT is synthesized stages of the by fetal 5-HT-ergic 5-HT system neurons are largely located comparable in the various between nuclei of humans and rodents. In humans, 5-HT-ergic neurons are first evident in the hindbrain at gestational the raphe nuclei in the brainstem and is transported into synaptic vesicles by the vesicular monoamine week 5 [16] after which they project to the forebrain, reaching the cerebral cortex around gestational transporter isoform 2. The exocytosis of these vesicles releases 5-HT into the synaptic cleft, where it binds week 10 and the most rostral telencephalon around gestational week 13 [17]. At gestational week 15, to post-synapticduring the second 5-HT receptors. trimester Thusof human far, at pregnancy, least 14 different the typical 5-HT or receptorganization subtypes of clustered have been 5-HT identified cell (5-HTbodies1A/B/D /intoE/F, 5-HTthe raphe2A/B/ Cnuclei, 5-HT is3 ,observed 5-HT4, 5-HT[18]. 5ASim/Bilarly,, 5-HT in6, rodents, and 5-HT 5-HT-positive7), which can cells trigger are observed a variety of signalingin the cascades. raphe nuclei All around but the embryonic 5-HT3 receptor day (E) are 10–1 metobotropic2, which corresponds and belong to the to second the G protein-coupledtrimester of receptorpregnancy superfamily. in humans. A complete One day overview after their of theappearance, receptor’s these transduction cells are able mechanisms to synthesize is beyond 5-HT [2]. the 5- scope of thisHT-ergic review andaxons has reach been discussedthe forebrain in detail in mice previously around [ 11E16.5,12]. Ofand note, in rats at the around cost of E17.5 5-HT, [19,20]. tryptophan can alsoInterestingly, serve as a precursor5-HT-ergic of signaling kynurenine molecules via the are rate-limiting already present enzymes in the tryptophan forebrain 2,3-dioxygenase before 5-HT-ergic (TDO) and indoleamineaxons reach it. 2,3-dioxygenase Human data show (IDO) the [13expression]. Kynurenine of 5-HTT is further in the brain degraded around into gestational multiple neuroactiveweek 8, metabolites,i.e., the first including trimester kynurenic of pregnanc acid andy [21]. quinolinic Similarly, acid. in mice The and kynurenine rats, brain pathway 5-HTT is plays detected a role around in immune E8-9 in the forebrain [2,22–24]. This suggests that an exogenous source may provide the fetal forebrain response and inflammation [14,15]. with 5-HT before the actual 5-HT-ergic projections reach the forebrain. FigureFigure 1. An 1. An integrated integrated view view ofof 5-HT signaling signaling within within the thebrain. brain. 5-HT 5-HTin the brain in the is brainsynthesized is synthesized from fromtryptophan tryptophan via via the theenzymes enzymes Tph2 Tph2and AADC. and AADC. 5-HT is 5-HTtransported is transported via VMAT viainto VMAT synaptic into vesicles. synaptic vesicles.Exocytosis Exocytosis of these of vesicles these vesicles releases releases5-HT into 5-HT the synaptic into the cleft. synaptic Here, cleft.it can Here,bind to it 5-HT can bindreceptors to 5-HT receptors localized on pre- and postsynaptic neurons and/or on glial cells (microglia, astrocytes, and oligodendrocytes). 5-HT signaling can be terminated by the reuptake of 5-HT via the 5-HT transporter. 5-HT is again transported into synaptic vesicles or converted to 5-HIAA via the enzyme MAOA. Within neurons, microglia, and astrocytes, tryptophan can be converted into kynurenine via the enzymes IDO and TDO. 5-HIAA: 5-hydroxyindole amino acid; 5-HT: serotonin; AADC: aromatic L-amino acid decarboxylase; IDO: indoleamine 2,3-dioxygenase; MAOA: monoamine oxidase A; TDO: tryptophan 2,3-dioxygenase; TPH2: tryptophan hydroxylase 2; VMAT: vesicular monoamine transporter.
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