Neurotrophin-3- and norepinephrine-mediated adrenergic differentiation and the inhibitory action of desipramine and cocaine

Zhang, Jianmin; Dix, Jessica; Langtimm-Sedlak, Carol J.; Trusk, Thomas C.; Schroeder, Brett; Hoffmann, Raymond G.; Strosberg, Aldo D.; Winslow, John; Sieber‐Blum, Maya

doi:10.1002/(sici)1097-4695(199703)32:3<262::aid-neu2>3.0.co;2-5

Cited by 29 publications

(3 citation statements)

References 81 publications

(29 reference statements)

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“…Studies have also shown that norepinephrine influences neural crest cell formation and differentiation during embryogenesis (Zhang et al, 1997;Sieber-Blum and Ren, 2000;Ren et al, 2001;Ren et al, 2003;Hu et al, 2009). Thus, if venlafaxine is taken during early pregnancy and interferes with these embryologic signaling pathways, it is plausible that venlafaxine could affect craniofacial and cardiac development.…”

Section: Discussionmentioning

confidence: 99%

Association between reported venlafaxine use in early pregnancy and birth defects, national birth defects prevention study, 1997–2007

Polen

Rasmussen

Riehle‐Colarusso

et al. 2012

Birth Defects Research

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BACKGROUND: Few epidemiologic studies have investigated the use of venlafaxine (Effexor XR capsules, Product Monograph, Wyeth, Montreal, Canada), an antidepressant used to treat major depression and anxiety disorders in adults, during pregnancy. Our objective was to determine whether use of venlafaxine during pregnancy is associated with specific birth defects. METHODS: We used data from the National Birth Defects Prevention Study (NBDPS), a population-based, case-control study in the United States. Our analysis included mothers with pregnancies affected by one of 30 selected birth defects (cases) and babies without birth defects (controls) with estimated dates of delivery between 1997 and 2007. Exposure was any reported use of venlafaxine from 1 month preconception through the third month of pregnancy. We calculated adjusted odds ratios (aORs) and 95% Fisher Exact confidence intervals (CIs) for 24 birth defect groups for which at least 400 case mothers were interviewed. Our adjusted analyses controlled for maternal age and race/ethnicity. RESULTS: Among the 27,045 NBDPS participants who met inclusion criteria, 0.17% (14/8002) of control mothers and 0.40% (77/19,043) of case mothers reported any use of venlafaxine from 1 month preconception through the third month of pregnancy. Statistically significant associations were found for anencephaly, atrial septal defect (ASD) secundum, or ASD not otherwise specified, coarctation of the aorta, cleft palate, and gastroschisis. CONCLUSIONS: Our data suggest associations between periconceptional use of venlafaxine and some birth defects. However, sample sizes were small, CIs were wide, and additional studies are needed to confirm these results. Birth Defects Research (Part A) 97: 28-35, 2013. Ó 2012

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Section: Discussionmentioning

confidence: 99%

Association between reported venlafaxine use in early pregnancy and birth defects, national birth defects prevention study, 1997–2007

Polen

Rasmussen

Riehle‐Colarusso

et al. 2012

Birth Defects Research

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“…In early embryonic development NET is distributed in a wide range of neuronal and nonneuronal tissues (Sieber-Blum and Ren, 2000). NET is believed to have additional functions such as specification of the neuronal norardrenergic phenotype as well as the differentiation of neural crest stem cells into sympathetic neurons (Zhang et al, 1997b;Zhang and Sieber-Blum, 1992;Renn et al, 2001;Kim et al, 2002). HoxA5 has been shown to recognize a HBS sequence within the promoter of the human (h) NET gene in vitro, through which it transactivates expression of a reporter gene (Kim et al, 2002).…”

Section: Norepinephrine Transporter Gene (Net)mentioning

confidence: 99%

Hox Genes and Their Candidate Downstream Targets in the Developing Central Nervous System

Akin

Nazarali

2005

Cell Mol Neurobiol

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1. Homeobox (Hox) genes were originally discovered in the fruit fly Drosophila, where they function through a conserved homeodomain as transcriptional regulators to control embryonic morphogenesis. Since then over 1000 homeodomain proteins have been identified in several species. In vertebrates, 39 Hox genes have been identified as homologs of the original Drosophila complex, and like their Drosophila counterparts they are organized within chromosomal clusters. Vertebrate Hox genes have also been shown to play a critical role in embryonic development as transcriptional regulators. 2. Both the Drosophila and vertebrate Hox genes have been shown to interact with various cofactors, such as the TALE homeodomain proteins, in recognition of consensus sequences within regulatory elements of their target genes. These protein-protein interactions are believed to contribute to enhancing the specificity of target gene recognition in a cell-type or tissue- dependent manner. The regulatory activity of a particular Hox protein on a specific regulatory element is highly variable and dependent on its interacting partners within the transcriptional complex. 3. In vertebrates, Hox genes display spatially restricted patterns of expression within the developing CNS, both along the anterioposterior and dorsoventral axis of the embryo. Their restricted gene expression is suggestive of a regulatory role in patterning of the CNS, as well as in cell specification. Determining the precise function of individual Hox genes in CNS morphogenesis through classical mutational analyses is complicated due to functional redundancy between Hox genes. 4. Understanding the precise mechanisms through which Hox genes mediate embryonic morphogenesis requires the identification of their downstream target genes. Although Hox genes have been implicated in the regulation of several pathways, few target genes have been shown to be under their direct regulatory control. Development of methodologies used for the isolation of target genes and for the analysis of putative targets will be beneficial in establishing the genetic pathways controlled by Hox factors. 5. Within the developing CNS various cell adhesion molecules and signaling molecules have been identified as candidate downstream target genes of Hox proteins. These targets play a role in processes such as cell migration and differentiation, and are implicated in contributing to neuronal processes such as plasticity and/or specification. Hence, Hox genes not only play a role in patterning of the CNS during early development, but may also contribute to cell specification and identity.

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“…3f). Most of these colonies also contained cells expressing the high affinity norepinephrine transporter Zhang et al, 1997). They are thus thought to be formed by neurogenic cells that reside in a more advanced compartment of differentiation than the colony-forming cells giving rise to flattened unpigmented and mixed colonies.…”

Section: Culture Systemmentioning

confidence: 99%

Mitogenic and anti-proliferative signals for neural crest cells and the neurogenic action of TGF-β1

1997

Self Cite

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The influence of pertinent growth factors on proliferation and differentiation of quail neural crest cell was assessed by in vitro colony assay in a serum‐free (0.5% chick embryo‐extract supplemented) culture medium. The factors tested included basic fibroblast growth factor (bFGF; FGF‐2), neurotrophins, and transforming growth factor‐beta‐1 (TGF‐β). Both bFGF and neurotrophins are implicated in the development of the peripheral nervous system, whereas TGF‐β can affect cell differentiation and modulate the action of other growth factors. Bromodeoxyuridine (BrdU) incorporation indicated that bFGF is mitogenic to pluripotent neural crest cells (and/or their immediate progeny) and to committed melanogenic cells. However, this was not reflected in an increase in colony size. In contrast, colony size did increase when nerve growth factor (NGF) was present in addition to bFGF. This indicated either that both factors are required to initiate cell proliferation or that at least some bFGF‐exposed cells become dependent on neurotrophins for survival. Sequential addition of the factors showed that exposure to bFGF was required prior to the presence of a neurotrophin, thus favoring the latter possibility. All three neurotrophins tested, NGF, brain‐derived neurotrophic factor (BDNF), and neurotrophin‐3 (NT‐3), were capable of supporting survival of pluripotent neural crest cells (or their closely related progeny) in the presence of bFGF. In the absence of bFGF, neurotrophins did not affect colony size. Although the BrdU data indicated that bFGF is also a mitogen for committed melanogenic cells, the size of pigmented colonies did not change in the presence of bFGF alone or of bFGF plus a neurotrophin. This suggested that another, yet to be determined, factor is required for the survival of proliferating melanogenic cells. Colony assays were also performed in the presence and absence of TGF‐β, both alone and in combination with bFGF plus NGF. TGF‐β inhibited proliferation of both pluripotent neural crest cells (and/or their immediate derivatives) and of committed melanogenic cells, causing a decrease in colony size. When TGF‐β was added to the culture medium together with the bFGF/NGF combination, this also caused a significant decrease in colony size, similar to the one observed with TGF‐β alone. TGF‐β blocked proliferation even when the cells were exposed 24 to 48 hr to the bFGF/NGF combination prior to addition of TGF‐β. Neurogenesis increased significantly in the presence of TGF‐β. The number per colony of both adrenergic cells and sensory neuron precursors increased in TGF‐β‐treated neuroblast‐positive colonies. The following new insights were derived from this study: 1) basic FGF is a mitogen for pluripotent neural crest cells (and/or their immediate derivatives); 2) pluripotent and committed melanogenic neural crest cells that have been exposed to bFGF become dependent on trophic support; 3) all neurotrophins tested (NGF, BDNF or NT‐3) can fulfill the trophic requirement of bFGF‐exposed pluripotent cells, but no...

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Neurotrophin-3- and norepinephrine-mediated adrenergic differentiation and the inhibitory action of desipramine and cocaine

Cited by 29 publications

References 81 publications

Association between reported venlafaxine use in early pregnancy and birth defects, national birth defects prevention study, 1997–2007

Association between reported venlafaxine use in early pregnancy and birth defects, national birth defects prevention study, 1997–2007

Hox Genes and Their Candidate Downstream Targets in the Developing Central Nervous System

Mitogenic and anti-proliferative signals for neural crest cells and the neurogenic action of TGF-β1

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