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¹ Laboratoire de Dysrégulations Métaboliques Acquises et Génétiques, UPRES EA 3901, Faculté de Médecine, Université de Picardie Jules Verne, 3 rue des Louvels, 80036 Amiens cedex 1, France
² Laboratoire de Neuropeptides Centraux et Régulations Hydrique et Cardiovasculaire, Inserm-U691, Collège de France, 11 place Marcelin Berthelot, 75231 Paris cedex 05, France
³ Laboratoire de Neurobiologie Génétique et Intégrative, CNRS UPR 2216, Institut de Neurobiologie Alfred Fessard, Avenue de la Terrasse, 91198 Gif-sur-Yvette, France

The ventral medullary surface (VMS) is a region known to exert a respiratory stimulant effect during hypercapnia. Several studies have suggested its involvement in the central inhibition of respiratory rhythm caused by hypoxia. We studied brainstem–spinal cord preparations isolated from newborn rats transiently superfused with a very low O₂ medium, causing reversible respiratory depression, to characterize the participation of the VMS in hypoxic respiratory adaptation. In the presence of 0.8 mM Ca²⁺, very low O₂ medium induced an increase in c-fos expression throughout the VMS. The reduction of synaptic transmission and blockade of the respiratory drive by 0.2 mM Ca²⁺–1.6 mM Mg²⁺ abolished c-fos expression in the medial VMS (at the lateral edge of the pyramidal tract) but not in the perifacial retrotrapezoid nucleus/parafacial respiratory group (RTN/pFRG) VMS, suggesting the existence of perifacial RTN/pFRG hypoxia-sensing neurons. In the presence of Ca²⁺ (0.8 mM), lesioning experiments suggested a physiological difference in perifacial RTN/pFRG VMS between the lateral VMS (beneath the ventrolateral part of the facial nucleus) and the middle VMS (beneath the ventromedial part of the facial nucleus), at least in newborn rats. The lateral VMS lesion, corresponding principally to the most rostral part of the pFRG, produced hypoxia-induced stimulation, whereas the middle VMS lesion, corresponding to the main part of the RTN, abolished hypoxic excitation. This may involve relay via the medial VMS, which is thought to be the parapyramidal group.

(Received 16 April 2006; accepted after revision 8 August 2006; first published online 10 August 2006)
Corresponding author L. Bodineau: Laboratoire de Dysrégulations Métaboliques Acquises et Génétiques, UPRES EA 3901, Faculté de Médecine, Université de Picardie Jules Verne, 3 rue des Louvels, 80036 Amiens cedex 1, France. Email: laurence.bodineau{at}u-picardie.fr

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