Serotonin uptake in the ectoplacental cone and placenta of the mouse

Yavarone, Mark; Shuey, Dana L.; Sadler, T. W.; Lauder, Jean M.

doi:10.1016/s0143-4004(05)80257-7

Cited by 95 publications

(63 citation statements)

References 27 publications

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“…The source of serotonin in pre-implantation embryos could be due to synthesis or uptake from extracellular sources (Yavarone et al 1993). Of the genes involved in synthesis, we could only detect the presence of Tph2 transcripts in the oocyte and the two-cell embryo and, therefore, we conclude that it is TPH2 that is active in the early embryo.…”

Section: Discussionmentioning

confidence: 68%

“…This PCR-based assay could also detect a minimum of 10 femtograms. These results indicate that serotonin present in embryos could arise either through synthesis by TPH2 or by transport from extracellular sources, for example, serotonin present in the tubal fluid of the oviduct (Juorio et al 1989, Amenta et al 1992, Yavarone et al 1993. The multiplicity of the mechanisms for obtaining serotonin may indicate the importance of this molecule to the embryo.…”

Section: Serotonin In Mitochondria In Mouse Embryosmentioning

confidence: 92%

“…In mammals, such studies have been lacking, though in mice, drastic effects are observed in the early embryo upon blocking tryptophan hydroxylase, the rate-limiting enzyme in serotonin synthesis. Serotonin is present in the tubal fluid of the oviduct, cervix, and uterus (Juorio et al 1989, Amenta et al 1992, Yavarone et al 1993). On administering p-chlorophenylalanine, a tryptophan hydroxylase inhibitor, to pregnant mice, it was observed that the cleavage divisions of the zygote were arrested and in cases where the embryo proceeded to the blastocyst stage, it was defective and failed to implant (Khozhai et al 1995).…”

Section: Introductionmentioning

confidence: 99%

“…The embryo may obtain serotonin either by synthesis and/or by uptake from its surrounding milieu (Yavarone et al 1993). The contribution of these two processes may also vary through early development.…”

Section: Introductionmentioning

confidence: 99%

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Serotonin in pre-implantation mouse embryos is localized to the mitochondria and can modulate mitochondrial potential

Basu¹,

Desai²,

Balaji³

et al. 2008

Reproduction

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Serotonin is reported to be present in early embryos of many species and plays an important role in early patterning. Since it is a fluorophore, it can be directly visualized using fluorescence microscopy. Here, we use three-photon microscopy to image serotonin in live pre-implantation mouse embryos. We find that it is present as puncta averaging 1.3 square microns and in concentrations as high as 442 mM. The observed serotonin puncta were found to co-localize with mitochondria. Live embryos pre-incubated with serotonin showed a higher mitochondrial potential, indicating that it can modulate mitochondrial potential. Pre-implantation mouse embryos were also examined at various developmental stages for the presence of transcripts of the peripheral and neuronal forms of tryptophan hydroxylase (Tph1 and Tph2 respectively) and the classical serotonin transporter (Slc6a4). Transcripts of Tph2 were seen in oocytes and in two-cell stages, whereas transcripts of Tph1 were not detected at any stage. Transcripts of the transporter, Slc6a4, were present in all pre-implantation stages investigated. These results suggest that serotonin in embryos can arise from a combination of synthesis and uptake from the surrounding milieu.

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Section: Discussionmentioning

confidence: 68%

Section: Serotonin In Mitochondria In Mouse Embryosmentioning

confidence: 92%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Serotonin in pre-implantation mouse embryos is localized to the mitochondria and can modulate mitochondrial potential

Basu¹,

Desai²,

Balaji³

et al. 2008

Reproduction

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show abstract

“…The first and most important source is the mother: maternal 5-HT is actively transported through the placental brush border cells via SERT (Cool et al, 1990;Carrasco et al, 2000). 5-HT immunostaining is present in the placenta and the ectoplacental cone (Yavarone et al, 1993). Raphe neuron differentiation and production of 5-HT starts by E10.5 in mice (Hendricks et al, 1999) and by the fifth gestational week in humans (Sundstrom et al, 1993;Verney et al, 2002;Paterson and Darnall, 2009).…”

Section: -Ht Sources During Developmentmentioning

confidence: 99%

Genetic Models of Serotonin (5‐HT) Depletion: What do They Tell Us About the Developmental Role of 5‐HT?

Trowbridge¹,

Narboux-Nême²,

Gaspar³

2010

The Anatomical Record

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A large number of hyposerotonergic genetic models have been generated over the past few years. Serotonin (5-HT) depletion has been obtained via targeting of genes involved in 5-HT synthesis (Tph1 and Tph2), specification and determination of the 5-HT phenotype during development (GATA3, Pet1, and Lmx1b), and 5-HT storage or clearance (Vmat2 and SERT). Here we review these various models from a developmental perspective, beginning with a description of the sources of 5-HT during development. We then summarize the neurological and behavioral alterations that have been observed in the genetic hyposerotonergic models. Although these models appear to have normal brain development and do not exhibit any gross morphological defects, problems in somatic growth and physiological functions have been observed. Abnormal adult behavior is also seen, although whether it results from depletion of 5-HT during development or functional 5-HT deficiencies in adult life remains unclear. Evidence from these hyposerotonergic models suggests that the developing brain may not need 5-HT for the establishment of general organization and structure. However, central 5-HT appears to be necessary for postnatal body growth, maturation of respiratory and vegetative control, and possibly for the development of normal adult behavior. Anat Rec, 294:1615Rec, 294: -1623Rec, 294: , 2011. V V C 2011 Wiley-Liss, Inc.

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Magnetic resonance microscopy in cardiac development

Smith

2001

Microsc. Res. Tech.

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Magnetic resonance microscopy (MRM) is a fast and non-destructive imaging technique that can analyze the three-dimensional structure of the embryonic heart both qualitatively and quantitatively. Intravascular contrast agents have been developed to accentuate the anatomy of cardiac chambers, the cardiac outflow tract, and major arteries and veins throughout the embryonic body. MRM generates non-distorted three-dimensional data of vascular anatomy in a fraction of the time required by conventional optical image reconstruction techniques. The three-dimensional nature of these data allows the creation of visual models that can be manipulated for fast and easy interpretation of the complex relationships between heart chambers and aortic arches. This is particularly helpful because these relationships change in complex ways during development. The non-destructive nature of MRM makes it well suited for investigating rare or valuable specimens and live subjects. MRM techniques have been developed for imaging the embryo in utero and in vitro, although MRM studies of fixed embryo specimens are easier to perform and produce data with better contrast and higher resolution.

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Serotonin uptake in the ectoplacental cone and placenta of the mouse

Cited by 95 publications

References 27 publications

Serotonin in pre-implantation mouse embryos is localized to the mitochondria and can modulate mitochondrial potential

Serotonin in pre-implantation mouse embryos is localized to the mitochondria and can modulate mitochondrial potential

Genetic Models of Serotonin (5‐HT) Depletion: What do They Tell Us About the Developmental Role of 5‐HT?

Magnetic resonance microscopy in cardiac development

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