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The Journal of Neuroscience, June 15, 2000, 20(12):4646-4656

Abnormal Phrenic Motoneuron Activity and Morphology in Neonatal Monoamine Oxidase A-Deficient Transgenic Mice: Possible Role of a Serotonin Excess

Céline Bou-Flores¹, Anne-Marie Lajard², Roger Monteau², Edward De Maeyer⁴, Isabelle Seif⁴, Jeanne Lanoir³, and Gérard Hilaire¹

¹ Unité Propre de Recherche (UPR) 9011, Development and Pathology of Movement, ² Unité Propre de Recherche et de l'Enseignement Supérieur 6034, Laboratoire Neurobiologie des Fonctions Végétatives, and ³ UPR 9024, Laboratoire de Neurobiologie, Centre National de la Recherche Scientifique (CNRS), Marseille Cedex 20, France, and ⁴ Unité Mixte de Recherche 146, CNRS, Institut Curie, 91405 Orsay, France

In rodent neonates, the neurotransmitter serotonin (5-HT) modulates the activity of both the medullary respiratory rhythm generator and the cervical phrenic motoneurons. To determine whether 5-HT also contributes to the maturation of the respiratory network, experiments were conducted in vitro on the brainstem-spinal cord preparation of neonatal mice originating from the control strain (C3H) and the monoamine oxidase A-deficient strain, which has a brain perinatal 5-HT excess (Tg8). At birth, the Tg8 respiratory network is unable to generate a respiratory pattern as stable as that produced by the C3H network, and the modulation by 5-HT of the network activity present in C3H neonates is lacking in Tg8 neonates. In addition, the morphology of the phrenic motoneurons is altered in Tg8 neonates; the motoneuron dendritic tree loses the C3H bipolar aspect but exhibits an increased number of spines and varicosities. These abnormalities were prevented in Tg8 neonates by treating pregnant Tg8 dams with the 5-HT synthesis inhibitor p-chlorophenylalanine or a 5-HT_2A receptor antagonist but were induced in wild-type neonates by treating C3H dams with a 5-HT_2A receptor agonist. We conclude that 5-HT contributes, probably via 5-HT_2A receptors, to the normal maturation of the respiratory network but alters it when present in excess. Disorders affecting 5-HT metabolism during gestation may therefore have deleterious effects on newborns.

Key words: serotonin; serotonergic receptors; medullary respiratory network; electrophysiology of phrenic motoneurons; morphology of phrenic motoneurons; fetal mice; neonatal mice; maturation; modulation of neonatal respiratory activity

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Copyright © 2000 Society for Neuroscience  0270-6474/00/20124646-11$05.00/0

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