Serotonin as a regulator of craniofacial morphogenesis: Site specific malformations following exposure to serotonin uptake inhibitors

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

doi:10.1002/tera.1420460407

Cited by 151 publications

(121 citation statements)

References 23 publications

Supporting

Mentioning

111

Contrasting

Unclassified

Order By: Relevance

“…Interestingly, the avian notochord has been shown to synthesize NE and other neurotransmitters before the emergence of any differentiated neurons in the central or peripheral nervous systems (Strudel et al, 1977). Moreover, serum and embryonic tissues contain nanomolar to micromolar amounts of NE and other neurotransmitters (Zhang and SieberBlum, 1992), which are thought to originate in the maternal bloodstream and enter the fetal bloodstream by crossing the placenta (Shuey et al, 1992). This observation and studies with adrenergic receptor agonists and antagonists (Zhang et al, 1997b) confirm that NE transport, rather than activation of adrenergic receptors, is responsible for promoting noradrenergic differentiation.…”

Section: A Role Of the Norepinephrine Transporter (Net) In Heart Devementioning

confidence: 97%

Cardiac neural crest stem cells

Sieber‐Blum

2003

Anat. Rec.

View full text Add to dashboard Cite

Whereas the heart itself is of mesodermal origin, components of the cardiac outflow tract are formed by the neural crest, an ectodermal derivative that gives rise to the peripheral nervous system, endocrine cells, melanocytes of the skin and internal organs, and connective tissue, bone, and cartilage of the face and ventral neck, among other tissues. Cardiac neural crest cells participate in the septation of the cardiac outflow tract into aorta and pulmonary artery. The migratory cardiac neural crest consists of stem cells, fate-restricted cells, and cells that are committed to the smooth muscle cell lineage. During their migration within the posterior branchial arches, the developmental potentials of pluripotent neural crest cells become restricted. Conversely, neural crest stem cells persist at many locations, including in the cardiac outflow tract. Many aspects of neural crest cell differentiation are driven by growth factor action. Neurotrophin-3 (NT-3) and its preferred receptor, TrkC, play important roles not only in nervous system development and function, but also in cardiac development as deletion of these genes causes outflow tract malformations. In vitro clonal analysis has shown a premature commitment of cardiac neural crest stem cells in TrkC null mice and a perturbed morphology of the endothelial tube. Norepinephrine transporter (NET) function promotes the differentiation of neural crest stem cells into noradrenergic neurons. Surprisingly, many diverse nonneuronal embryonic tissues, in particular in the cardiovascular system, express NET also. It will be of interest to determine whether norepinephrine transport plays a role also in cardiovascular development. Anat Rec Part A 276A: 34 -42, 2004.

show abstract

Section: A Role Of the Norepinephrine Transporter (Net) In Heart Devementioning

confidence: 97%

Cardiac neural crest stem cells

Sieber‐Blum

2003

Anat. Rec.

View full text Add to dashboard Cite

show abstract

“…This mechanism allows the tissues to buffer 5-HT levels by modulating 5-HT uptake and release. Uptake of 5-HT during early development is first observed in non-neuronal tissues such as the heart, the liver, the cranial mesenchyme, and the notochord (Lauder and Zimmerman, 1988;Shuey et al, 1992;Pavone et al, 2008). Later, 5-HT accumulation is detected in several categories of neurons, both in the brain and in neural crest derivatives (Hansson et al, 1999;NarbouxNeme et al, 2008).…”

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

View full text Add to dashboard Cite

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.

show abstract

“…Some studies on mouse embryo cultures treated with serotonin suggest an improved development of serotoninergic cells in the nervous tissue and of cells of the nasal prominence, epithelium covering the eye, optic vesicle, and oral cavity (10,(29)(30)(31)(32)(33). These findings indicate that serotonin plays a role in the control of the epithelial-mesenchymal interactions during craniofacial morphogenesis (26). Serotoninergic treatment also caused malformation of both nerve and bone structures of mouse embryos (10).…”

Section: Discussionmentioning

confidence: 97%

“…In addition, there is evidence that SSRI and some serotoninergic agonists also increase 5-HT release not only in neuronal tissues (10,11,25) but also in non-neuronal tissues (26,27). Interestingly, serotonin has a trophic action on the differentiation of sev- Kruskal-Wallis analysis of variance followed by the Dunn test were used to compare physical features between each citalopram dose and the saline control group.…”

Section: Discussionmentioning

confidence: 99%

Neonatal administration of citalopram delays somatic maturation in rats

Deiró

Manhães-de-Castro

Cabral-Filho³

et al. 2004

Braz J Med Biol Res

View full text Add to dashboard Cite

We investigated the somatic maturation of neonate rats treated during the suckling period with citalopram, a selective serotonin reuptake inhibitor. Groups with 6 male neonates were randomly assigned to different treatments 24 h after birth. Each litter was suckled by one of the dams until the 21st postnatal day. Body weight, head axis and tail length were measured daily from the 1st to the 21st postnatal day. Time of ear unfolding, auditory conduit opening, incisor eruption, and eye opening was determined. Pups received 5 mg (Cit5), 10 mg (Cit10) or 20 mg/kg (Cit20) citalopram sc, or saline (0.9% NaCl, w/v, sc). Compared to saline, body weight was lower (24.04%, P < 0.01) for Cit10 from the 10th to the 21st day and for Cit20 from the 6th to the 21st day (38.19%, P < 0.01). Tail length was reduced in the Cit20 group (15.48%, P < 0.001) from the 8th to the 21st day. A reduction in mediolateral head axis (10.53%, P < 0.05) was observed from the 11th to the 21st day in Cit10 and from the 6th to the 21st day in Cit20 (13.16%, P < 0.001). A reduction in anteroposterior head axis was also observed in the Cit20 group (5.28%, P < 0.05) from the 13th to the 21st day. Conversely, this axis showed accelerated growth from the 12th to the 21st day in the Cit5 group (13.05%, P < 0.05). Auditory conduit opening was delayed in the Cit5 and Cit20 groups and incisor eruption was delayed in all citalopram groups. These findings show that citalopram injected during suckling to rats induces body alterations and suggest that the activity of the serotoninergic system participates in growth mechanisms.

show abstract

Serotonin as a regulator of craniofacial morphogenesis: Site specific malformations following exposure to serotonin uptake inhibitors

Cited by 151 publications

References 23 publications

Cardiac neural crest stem cells

Cardiac neural crest stem cells

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

Neonatal administration of citalopram delays somatic maturation in rats

Contact Info

Product

Resources

About