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Excess of serotonin affects embryonic interneuron migration through activation of the serotonin receptor 6

RICCIO, O ; POTTER, G ; WALZER, C ; VALLET, P ; SZABO, G ; VUTSKITS, L ; KISS, J. Z ; DAYER, A. G

Molecular psychiatry, 2009-03, Vol.14 (3), p.280-290 [Periódico revisado por pares]

Basingstoke: Nature Publishing Group

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Título:
Excess of serotonin affects embryonic interneuron migration through activation of the serotonin receptor 6
Autor: RICCIO, O ; POTTER, G ; WALZER, C ; VALLET, P ; SZABO, G ; VUTSKITS, L ; KISS, J. Z ; DAYER, A. G
Assuntos: Adult and adolescent clinical studies ; Animals ; Biological and medical sciences ; Cell migration ; Cell Movement - drug effects ; Cell Movement - physiology ; Cerebral cortex ; Cerebral Cortex - cytology ; Cerebral Cortex - embryology ; Cerebral Cortex - physiology ; Critical Period (Psychology) ; Depression ; Depression, Mental ; Dose-Response Relationship, Drug ; Embryos ; Extracellular levels ; Gene polymorphism ; Genetic aspects ; Homeostasis ; Interneurons ; Interneurons - cytology ; Interneurons - metabolism ; Leukocyte migration ; Medical sciences ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mood disorders ; Organ Culture Techniques ; Psychology. Psychoanalysis. Psychiatry ; Psychopathology. Psychiatry ; Receptor mechanisms ; Receptors ; Receptors, Serotonin - metabolism ; Risk factors ; Serotonin ; Serotonin - administration & dosage ; Serotonin - physiology ; Serotonin Plasma Membrane Transport Proteins - genetics ; Serotonin Plasma Membrane Transport Proteins - metabolism ; Serotonin S6 receptors ; Serotonin transporter
É parte de: Molecular psychiatry, 2009-03, Vol.14 (3), p.280-290
Notas: ObjectType-Article-1
SourceType-Scholarly Journals-1
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Descrição: The discovery that a common polymorphism (5-HTTLPR, short variant) in the human serotonin transporter gene (SLC6A4) can influence personality traits and increase the risk for depression in adulthood has led to the hypothesis that a relative increase in the extracellular levels of serotonin (5-HT) during development could be critical for the establishment of brain circuits. Consistent with this idea, a large body of data demonstrate that 5-HT is a strong neurodevelopmental signal that can modulate a wide variety of cellular processes. In humans, serotonergic fibers appear in the developing cortex as early as the 10th gestational week, a period of intense neuronal migration. In this study we hypothesized that an excess of 5-HT could affect embryonic cortical interneuron migration. Using time-lapse videometry to monitor the migration of interneurons in embryonic mouse cortical slices, we discovered that the application of 5-HT decreased interneuron migration in a reversible and dose-dependent manner. We next found that 5-HT6 receptors were expressed in cortical interneurons and that 5-HT6 receptor activation decreased interneuron migration, whereas 5-HT6 receptor blockade prevented the migratory effects induced by 5-HT. Finally, we observed that interneurons were abnormally distributed in the cerebral cortex of serotonin transporter gene (Slc6a4) knockout mice that have high levels of extracellular 5-HT. These results shed new light on the neurodevelopmental alterations caused by an excess of 5-HT during the embryonic period and contribute to a better understanding of the cellular processes that could be modulated by genetically controlled differences in human 5-HT homeostasis.
Editor: Basingstoke: Nature Publishing Group
Idioma: Inglês

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Excess of serotonin affects embryonic interneuron migration through activation of the serotonin receptor 6

RICCIO, O ; POTTER, G ; WALZER, C ; VALLET, P ; SZABO, G ; VUTSKITS, L ; KISS, J. Z ; DAYER, A. G

Basingstoke: Nature Publishing Group

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