Nasal Trigeminal Inputs Release the A5 Inhibition Received by the Respiratory Rhythm Generator of the Mouse Neonate

• Published in: Journal of neurophysiology 2004-02, Vol.91 (2), p.746-758
• Main Authors: Viemari, Jean-Charles, Bevengut, Michelle, Coulon, Patrice, Hilaire, Gerard
• Format: Article
• Language: English
• Subjects: Afferent Pathways; Afferent Pathways - drug effects; Afferent Pathways - physiology; Animals; Animals, Newborn; Biochemistry; Biochemistry, Molecular Biology; Electric Stimulation; Electric Stimulation - methods; Life Sciences; Mice; Nasal Cavity; Nasal Cavity - drug effects; Nasal Cavity - physiology; Neural Inhibition; Neural Inhibition - drug effects; Neural Inhibition - physiology; Piperoxan; Piperoxan - pharmacology; Respiratory Mechanics; Respiratory Mechanics - drug effects; Respiratory Mechanics - physiology; Trigeminal Nerve; Trigeminal Nerve - drug effects; Trigeminal Nerve - physiology
• ISSN: 0022-3077; 1522-1598
• DOI: 10.1152/jn.01153.2002

Centre National de la Recherche Scientifique, Université de la Méditerranée, Groupe d'Étude des Réseaux Moteurs, Biologie des Rythmes et du Développement, 13009 Marseille, France Submitted 20 December 2002; accepted in final form 9 October 2003 Experiments were performed on neonatal mice to analyze why, in vitro, the respiratory rhythm generator (RRG) was silent and how it could be activated. We demonstrated that in vitro the RRG in intact brain stems is silenced by a powerful inhibition arising from the pontine A5 neurons through medullary 2 adrenoceptors and that in vivo nasal trigeminal inputs facilitate the RRG as nasal continuous positive airway pressure increases the breathing frequency, whereas nasal occlusion and nasal afferent anesthesia depress it. Because nasal trigeminal afferents project to the A5 nuclei, we applied single trains of negative electric shocks to the trigeminal nerve in inactive ponto-medullary preparations. They induced rhythmic phrenic bursts during the stimulation and for 2–3 min afterward, whereas repetitive trains produced on-going rhythmic activity up to the end of the experiments. Electrolytic lesion or pharmacological inactivation of the ipsilateral A5 neurons altered both the phrenic burst frequency and occurrence after the stimulation. Extracellular unitary recordings and trans -neuronal tracing experiments with the rabies virus show that the medullary lateral reticular area contains respiratory-modulated neurons, not necessary for respiratory rhythmogenesis, but that may provide an excitatory pathway from the trigeminal inputs to the RRG as their electrolytic lesion suppresses any phrenic activity induced by the trigeminal nerve stimulation. The results lead to the hypothesis that the trigeminal afferents in the mouse neonate involve at least two pathways to activate the RRG, one that may act through the medullary lateral reticular area and one that releases the A5 inhibition received by the RRG. Address reprint requests and other correspondence to: M. Bévengut, Centre National de la Recherche Scientifique, Université de la Méditerranée, Groupe d'Étude des Réseaux Moteurs, Biologie des Rythmes et du Développement, 280 Boulevard Sainte Marguerite, 13009 Marseille, France (E-mail: bevengut{at}marseille.inserm.fr ).