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78 Serotonin and S‐100: roles in development and adult plasticity
Author(s) -
WhitakerAzmitia P.M.,
Azmitia E.C.
Publication year - 1996
Publication title -
international journal of developmental neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.761
H-Index - 88
eISSN - 1873-474X
pISSN - 0736-5748
DOI - 10.1016/0736-5748(96)80273-5
Subject(s) - citation , library science , psychology , computer science
During mouse embryogenesis, serotonin (S-HT) uptake sites and receptors are expressed in craniofacial epithelia and mesenchyme. Serotonin appears to be derived from the matemalembryonic circulation in viw, whereas cultured embryos receive 5-HT from serum. Exposure of cultured embryos to uptake inhibitors or receptor ligands causes multiple craniofacial defects, including hypoplasia of the forebrain, nasal prominence, maxilla and mandible, and defective lens invagination. Based on these results, we have hypothesized that S-HT acts as a dose-dependent morphogenetic signal (morphogen) during mouse craniofacial development. Results of several studies support this hypothesis. Cranial neural crest cells, when placed in a chemofaxis chamber, respond to low doses of .5-HT by increased migration, mediated by 5-HT,, receptors. In chondrogenic mandilar micromass cultures, antagonists selective for 5-HT receptor subtypes differentially regulate expression of cartilage proteoglycan core protein, tenascin, S-lOOp, and insulin-like growth factors. In organotypic mandibular culhnes, tooth germ development is stimulated by S-HT in a dosedependent manner, which is mediated by uptake and receptors. Results of these studies suggest that 5-HT may be an important humoral factor for craniofacial morphogenesis. Supported by NIH grant HD 22052 to JML and a Dental Scientist Research Fellowship to JRDM.