Prenatal fluoxetine exposure induces life-long serotonin 5-HT3 receptor-dependent cortical abnormalities and anxiety-like behaviour

Smit-Rigter, Laura A.; Noorlander, C.W.; Oerthel, Lars von; Chameau, Pascal; Smidt, Marten P.; Hooft, Johannes A. van

doi:10.1016/j.neuropharm.2011.09.015

Cited by 77 publications

(62 citation statements)

References 29 publications

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“…A similar 5-HT sensitivity has been reported for layer 2/3 pyramidal neurons in the SSC, where increased 5-HT signaling from E8 to E18 decreases apical dendritic arborization (Chameau et al, 2009;Smit-Rigter et al, 2012). This latter effect is mediated by 5-HT 3A receptors present on reelin secreting Cajal-Retzius cells (Smit-Rigter et al, 2012), which upon activation stimulate the release of reelin, which in turn limits cortical neuron apical dendritic elaboration (Chameau et al, 2009;Smit-Rigter et al, 2011). As Cajal-Retzius cells are still present and active in the first two postnatal weeks, a similar mechanism involving hyperactivation of the 5-HT 3A receptors can be postulated for the cytoarchitectural changes observed following postnatal FLX treatment.…”

Section: Mechanistic Insight On the Postnatal Establishment Of Pertursupporting

confidence: 78%

“…Postnatal FLX treatment reduces the arborization of apical dendrites of layer 2/3 infralimbic (IL) but not prelimbic (PL) pyramidal neurons in mice (Rebello et al, 2014;Figure 2). A similar 5-HT sensitivity has been reported for layer 2/3 pyramidal neurons in the SSC, where increased 5-HT signaling from E8 to E18 decreases apical dendritic arborization (Chameau et al, 2009;Smit-Rigter et al, 2012). This latter effect is mediated by 5-HT 3A receptors present on reelin secreting Cajal-Retzius cells (Smit-Rigter et al, 2012), which upon activation stimulate the release of reelin, which in turn limits cortical neuron apical dendritic elaboration (Chameau et al, 2009;Smit-Rigter et al, 2011).…”

Section: Mechanistic Insight On the Postnatal Establishment Of Pertursupporting

confidence: 72%

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Monoamine-Sensitive Developmental Periods Impacting Adult Emotional and Cognitive Behaviors

Suri

Teixeira

Cagliostro

et al. 2014

Neuropsychopharmacol

141

125

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Development passes through sensitive periods, during which plasticity allows for genetic and environmental factors to exert indelible influence on the maturation of the organism. In the context of central nervous system development, such sensitive periods shape the formation of neurocircuits that mediate, regulate, and control behavior. This general mechanism allows for development to be guided by both the genetic blueprint as well as the environmental context. While allowing for adaptation, such sensitive periods are also vulnerability windows during which external and internal factors can confer risk to disorders by derailing otherwise resilient developmental programs. Here we review developmental periods that are sensitive to monoamine signaling and impact adult behaviors of relevance to psychiatry. Specifically, we review (1) a serotonin-sensitive period that impacts sensory system development, (2) a serotonin-sensitive period that impacts cognition, anxiety-and depressionrelated behaviors, and (3) a dopamine-and serotonin-sensitive period affecting aggression, impulsivity and behavioral response to psychostimulants. We discuss preclinical data to provide mechanistic insight, as well as epidemiological and clinical data to point out translational relevance. The field of translational developmental neuroscience has progressed exponentially providing solid conceptual advances and unprecedented mechanistic insight. With such knowledge at hand and important methodological innovation ongoing, the field is poised for breakthroughs elucidating the developmental origins of neuropsychiatric disorders, and thus understanding pathophysiology. Such knowledge of sensitive periods that determine the developmental trajectory of complex behaviors is a necessary step towards improving prevention and treatment approaches for neuropsychiatric disorders.

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Section: Mechanistic Insight On the Postnatal Establishment Of Pertursupporting

confidence: 78%

Section: Mechanistic Insight On the Postnatal Establishment Of Pertursupporting

confidence: 72%

Monoamine-Sensitive Developmental Periods Impacting Adult Emotional and Cognitive Behaviors

Suri

Teixeira

Cagliostro

et al. 2014

Neuropsychopharmacol

141

125

View full text Add to dashboard Cite

show abstract

“…Increased 5-HT-receptor activation leads to altered migration, 3,4 neural circuitry refinement, 5−7 and maturation of dendritic arbors. 8 Pharmacological depletion of 5-HT with agents such as the 5-HT synthesis inhibitor para-chlorophenylalanine (pCPA), or the neurotoxin 5,7-dihydroxytryptamine (5,7-DHT), administered during embryonic or postnatal development, were reported to have effects on the maturation of cortical neurons 9,10 and to alter barrel cortex development, 11,12 although this was not confirmed in other reports. 5, 13 However, such pharmacological treatments are difficult to interpret because they are generally not specific in that they affect both central and peripheral sources of 5-HT and can have unwanted side effects on other amines.…”

Section: * S Supporting Informationmentioning

confidence: 96%

Postnatal Growth Defects in Mice with Constitutive Depletion of Central Serotonin

Narboux-Nême

Angenard

Mosienko

et al. 2012

ACS Chem. Neurosci.

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Although the trophic actions of serotonin (5-HT) are well established, only few developmental defects have been reported in mouse strains with constitutive hyposerotonergia. We analyzed postnatal growth and cortical development in three different mutant mouse strains with constitutive reductions in central 5-HT levels. We compared two previously published mouse strains with severe (−95%) depletions of 5-HT, the tryptophan hydroxylase (Tph) 2 −/− mouse line and VMAT2 sert-cre mice, with a new strain, in which VMAT2 deletion is driven by Pet1 (VMAT2 pet1-cre ) in 5-HT raphe neurons leading to partial (−75%) reduction in brain 5-HT levels. We find that normal embryonic growth and postnatal growth retardation are common features of all these mouse strains. Postnatal growth retardation varied from mild to severe according to the extent of the brain 5-HT reduction and gender. Normal growth was reinstated in VMAT2 sert-cre mice by reconstituting central 5-HT stores. Growth abnormalities could not be linked to altered food intake or temperature control. Morphological study of the cerebral cortex over postnatal development showed a delayed maturation of the upper cortical layers in the VMAT2 sert-cre and Tph2 −/− mice, but not in the VMAT2 pet1-cre mice. No changes in layer-specific gene expression or morphological alterations of barrel cortex development were found. Overall, these observations sustain the notion that central 5-HT signaling is required for the preweaning growth spurt of mouse pups. Brain development appeared to be immune to severe central 5-HT depletion for its overall growth during prenatal life, whereas reduced brain growth and delayed cortical maturation development occurred during postnatal life. Reduced developmental 5-HT signaling during postnatal development might modulate the function and fine structure of neural circuits in ways that affect adult behavior.

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“…Such a role is specific to a selective developmental period and SSRIs have opposite functions at mature stages [194]. Furthermore, the effects of SSRIs on developing dendrites were abolished when administered in the 5-HT 3A :KO mice or after pharmacological blockade of the 5-HT 3A receptor [173,195]. Moreover, the fine tuning of 5-HT 3A signalling has been shown to be responsible for the anxiety-like behaviours that are induced by prenatal fluoxetine treatment in wild type mice [196].…”

Section: Serotonin and Dendritic Maturation Of Cortical Neuronsmentioning

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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Prenatal fluoxetine exposure induces life-long serotonin 5-HT3 receptor-dependent cortical abnormalities and anxiety-like behaviour

Cited by 77 publications

References 29 publications

Monoamine-Sensitive Developmental Periods Impacting Adult Emotional and Cognitive Behaviors

Monoamine-Sensitive Developmental Periods Impacting Adult Emotional and Cognitive Behaviors

Postnatal Growth Defects in Mice with Constitutive Depletion of Central Serotonin

Sculpting Cerebral Cortex with Serotonin in Rodent and Primate

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