[Neocortex formation in mice developing after prenatal serotonin depletion].
The objective of this study was a detailed investigation of structural changes taking place in murine neocortex during its formation and stratification after prenatal serotonin depletion. The study was carried out in murine embryos of F1 (C58BL/CBA) hybrid strain. For depletion of endogenous serotonin in mice, pchlorophenylalanin, an inhibitor of tryptophan hydroxylase - a key enzyme of serotonin synthesis, was used. Brain of the offspring was studied on postnatal days 1, 5 and 10 (n = 10-15 for each time point). Intact animals of respective developmental stages were used as a control. The study demonstrated that prenatal inhibition of serotonin synthesis resulted in malformation of all neocortical layers, disorders of neuronal growth, development and differentiation, changes in their shape and dimensions. During postnatal development, the loss of a significant numbers of cells was observed in the brain structures studied of serotonin-depleted animals.
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D000818:Animals; D002454:Cell Differentiation; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005260:Female; D010134:Fenclonine / Q000494:pharmacology; D051379:Mice; D008810:Mice, Inbred C57BL; D008808:Mice, Inbred CBA; D019579:Neocortex / Q000002:abnormalities* / Q000166:cytology / Q000196:embryology*; D009474:Neurons / Q000166:cytology / Q000378:metabolism; D012701:Serotonin / Q000172:deficiency*; D012702:Serotonin Antagonists / Q000494:pharmacology; D014365:Tryptophan Hydroxylase / Q000037:antagonists & inhibitors
D004791:Enzyme Inhibitors; D012702:Serotonin Antagonists; D012701:Serotonin; D014365:Tryptophan Hydroxylase; D010134:Fenclonine