Neurotransmitters as morphogens

Lauder, Jean M.

doi:10.1016/s0079-6123(08)60516-6

Cited by 235 publications

(111 citation statements)

References 96 publications

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“…In the adult, mature brain, increases in, or unusual patterns of, catecholamine activity may result in sensitization. In the developing brain, however, neurotransmitters, in addition to their roles in cellular communication, play an important role in the basic neurodevelopmental processes (Lauder 1988). Trauma-related alterations in catecholamine activity during childhood, therefore, may alter brain development, resulting in altered functional capabilities of the 'traumatized' brain.…”

Section: Neurodevelopment Factorsmentioning

confidence: 99%

Consensus paper of the WFSBP Task Force on Biological Markers: Biological Markers in Depression

Mößner

Mikova

Koutsilieri

et al. 2007

The World Journal of Biological Psychiatry

227

126

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Biological markers for depression are of great interest to aid in elucidating the causes of major depression. We assess currently available biological markers to query their validity for aiding in the diagnosis of major depression. We specifically focus on neurotrophic factors, serotonergic markers, biochemical markers, immunological markers, neuroimaging, neurophysiological findings, and neuropsychological markers. We delineate the most robust biological markers of major depression. These include decreased platelet imipramine binding, decreased 5-HT1A receptor expression, increase of soluble interleukin-2 receptor and interleukin-6 in serum, decreased brain-derived neurotrophic factor in serum, hypocholesterolemia, low blood folate levels, and impaired suppression of the dexamethasone suppression test. To date, however, none of these markers are sufficiently specific to contribute to the diagnosis of major depression. Thus, with regard to new diagnostic manuals such as DSM-V and ICD-11 which are currently assessing whether biological markers may be included in diagnostic criteria, no biological markers for major depression are currently available for inclusion in the diagnostic criteria.

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Section: Neurodevelopment Factorsmentioning

confidence: 99%

Consensus paper of the WFSBP Task Force on Biological Markers: Biological Markers in Depression

Mößner

Mikova

Koutsilieri

et al. 2007

The World Journal of Biological Psychiatry

227

126

View full text Add to dashboard Cite

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“…Therefore, a role for dopamine in brain development that may be independent of its role at the synapse in the mature brain appears likely [24,25,28,38]. Activation of dopamine receptors influences cell proliferation in the lateral ganglionic eminence (LGE) and the neuroepithelium of the frontal cortex in embryonic mice [39,43,72,73] and in the subventricular zone and hippocampal dentate gyrus in the adult mice [18,22,64].…”

Section: Introductionmentioning

confidence: 99%

Elevated dopamine levels during gestation produce region-specific decreases in neurogenesis and subtle deficits in neuronal numbers

2007

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Dopamine levels in the fetal brain were increased by administering the dopamine precursor 3,4-dihydroxy-L-phenylalanine (L-DOPA) to pregnant mice in drinking water. The L-DOPA exposure decreased bromodeoxyuridine (BrdU) labeling in the lateral ganglionic eminence and frontal cortical neuroepithelium but not medial or caudal ganglionic eminences. The regional differences appear to reflect heterogeneity in precursor cells' responses to dopamine receptor activation. Relative numbers of E15 generated neurons were decreased at postnatal day 21 (P21) in the caudate-putamen, nucleus accumbens and frontal cortex but not globus pallidus in the L-DOPA group. TUNEL labeling did not show significant differences on P0, P7 or P14 in the caudate-putamen or frontal cortex, suggesting that cell death was not altered. Although virtually all cells in the P21 brains that were labeled with the E15 BrdU injection were NeuN-positive, stereological analyses showed no significant changes in total numbers of NeuN-positive or NeuN-negative cells in the P21 caudate-putamen or frontal cortex. Thus persisting deficits in neuronal numbers were evident in the L-DOPA group only by birth-dating analyses and not upon gross histological examination of brain sections or analysis of total numbers of neurons or glia. One explanation for this apparent discrepancy is that L-DOPA exposure decreased cell proliferation at E15 but not at E13. By E15, expansion of the neuroepithelial precursor pool is complete and any decrease in cell proliferation likely produces only marginal decreases in the total numbers of cells generated. Our L-DOPA exposure model may be pertinent to investigations of neurological dysfunction produced by developmental dopamine imbalance.

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“…Independently of its location in adults, 5-HT also has been detected during zygotic cleavage divisions, gastrulation and neurulation in embryos of sea urchins, frogs, chicken, and Drosophila. The presence of 5-HT and its receptors in early embryogenesis and the ability of 5-HTspecific pharmacological agents (5) to interfere with embryonic development suggested that early embryos use 5-HT before the onset of neurogenesis to regulate cell proliferation and͞or morphogenetic movements (6,7). Furthermore, 5-HT has been suspected for years to regulate craniofacial and cardiovascular morphogenesis: In embryos grown in the presence of either a high concentration of 5-HT or 5-HT-specific reuptake inhibitors, a decreased proliferation of myocardium, cardiac mesenchyme, and endothelium has been reported, indicating that 5-HT may regulate proliferation in the embryonic heart (8).…”

mentioning

confidence: 99%

Serotonin 2B receptor is required for heart development

Nebigil

Choi

Dierich

et al. 2000

Proc. Natl. Acad. Sci. U.S.A.

285

211

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Several lines of evidence suggest that the serotonin (5-hydroxytryptamine, 5-HT) regulates cardiovascular functions during embryogenesis and adulthood. 5-HT binds to numerous cognate receptors to initiate its biological effects. However, none of the 5-HT receptor disruptions in mice have yet resulted in embryonic defects. Here we show that 5-HT 2B receptor is an important regulator of cardiac development. We found that inactivation of 5-HT2B gene leads to embryonic and neonatal death caused by heart defects. 5-HT 2B mutant embryos exhibit a lack of trabeculae in the heart and a specific reduction in the expression levels of a tyrosine kinase receptor, ErbB-2, leading to midgestation lethality. These in vivo data suggest that the Gq-coupled receptor 5-HT 2B uses the signaling pathway of tyrosine kinase receptor ErbB-2 for cardiac differentiation. All surviving newborn mice display a severe ventricular hypoplasia caused by impaired proliferative capacity of myocytes. In adult mutant mice, cardiac histopathological changes including myocyte disarray and ventricular dilation were consistently observed. Our results constitute genetic evidence that 5-HT via 5-HT2B receptor regulates differentiation and proliferation of developing and adult heart. This mutation provides a genetic model for cardiopathy and should facilitate studies of both the pathogenesis and therapy of cardiac disorders in humans.neuregulin ͉ knockout ͉ proliferation ͉ transactivation S erotonin (5-hydroxytryptamine) (5-HT) first isolated as a vasoconstrictor from blood was later identified in the central nervous system (CNS). It is found in three main areas of the body: the intestinal wall, platelets, and CNS. The functions of 5-HT in CNS as a neurotransmitter are numerous and appear to involve control of appetite, sleep, memory and learning, temperature regulation, mood, behavior (including sexual and hallucinogenic behavior), and endocrine regulation (1). Peripherally, 5-HT, which is stored in platelets, appears to play a major role in homeostasis, blood pressure regulation, cardiovascular functions (2), motility of the gastrointestinal tract (3), and carcinoid tumor pathology (4). Independently of its location in adults, 5-HT also has been detected during zygotic cleavage divisions, gastrulation and neurulation in embryos of sea urchins, frogs, chicken, and Drosophila. The presence of 5-HT and its receptors in early embryogenesis and the ability of 5-HTspecific pharmacological agents (5) to interfere with embryonic development suggested that early embryos use 5-HT before the onset of neurogenesis to regulate cell proliferation and͞or morphogenetic movements (6, 7). Furthermore, 5-HT has been suspected for years to regulate craniofacial and cardiovascular morphogenesis: In embryos grown in the presence of either a high concentration of 5-HT or 5-HT-specific reuptake inhibitors, a decreased proliferation of myocardium, cardiac mesenchyme, and endothelium has been reported, indicating that 5-HT may regulate proliferation in the embryonic heart (8).Th...

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Neurotransmitters as morphogens

Cited by 235 publications

References 96 publications

Consensus paper of the WFSBP Task Force on Biological Markers: Biological Markers in Depression

Consensus paper of the WFSBP Task Force on Biological Markers: Biological Markers in Depression

Elevated dopamine levels during gestation produce region-specific decreases in neurogenesis and subtle deficits in neuronal numbers

Serotonin 2B receptor is required for heart development

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