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Fluoxetine treatment abolishes the in vitro respiratory response to acidosis in neonatal mice

By Nicolas Voituron, Yuri Shvarev, Clément Menuet, Michelle Bevengut, Caroline Fasano, Erika Vigneault, Salah El Mestikawy and Gérard Hilaire


International audienceBACKGROUND: To secure pH homeostasis, the central respiratory network must permanently adapt its rhythmic motor drive to environment and behaviour. In neonates, it is commonly admitted that the retrotrapezoid/parafacial respiratory group of neurons of the ventral medulla plays the primary role in the respiratory response to acidosis, although the serotonergic system may also contribute to this response.METHODOLOGY/PRINCIPAL FINDINGS: Using en bloc medullary preparations from neonatal mice, we have shown for the first time that the respiratory response to acidosis is abolished after pre-treatment with the serotonin-transporter blocker fluoxetine (25-50 µM, 20 min), a commonly used antidepressant. Using mRNA in situ hybridization and immunohistology, we have also shown the expression of the serotonin transporter mRNA and serotonin-containing neurons in the vicinity of the RTN/pFRG of neonatal mice.CONCLUSIONS: These results reveal that the serotonergic system plays a pivotal role in pH homeostasis. Although obtained in vitro in neonatal mice, they suggest that drugs targeting the serotonergic system should be used with caution in infants, pregnant women and breastfeeding mothers

Topics: Neonates, Infants, Brainstem, Breathing, Acidosis, Neurons, Serotonin, Mouse models, MESH: Acidosis, MESH: Animals, MESH: In Situ Hybridization, MESH: Mice, MESH: Mice, Inbred BALB C, MESH: RNA, Messenger, MESH: Respiration, MESH: Serotonin, MESH: Serotonin Plasma Membrane Transport Proteins, MESH: Serotonin Uptake Inhibitors, MESH: Animals, Newborn, MESH: Base Sequence, MESH: DNA Primers, MESH: Fluoxetine, [SDV.NEU.NB]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Neurobiology
Publisher: 'Public Library of Science (PLoS)'
Year: 2010
DOI identifier: 10.1371/journal.pone.0013644
OAI identifier: oai:HAL:hal-00625245v1
Provided by: HAL AMU
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