Voituron N, Frugière A, Champagnat J, Bodineau L
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.
J Physiol. 2006 Nov 15;577(Pt 1):55-68. doi: 10.1113/jphysiol.2006.111765. Epub 2006 Aug 10.
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 O(2) medium, causing reversible respiratory depression, to characterize the participation of the VMS in hypoxic respiratory adaptation. In the presence of 0.8 mM Ca(2+), very low O(2) 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 Ca(2+)-1.6 mM Mg(2+) 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 Ca(2+) (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.
延髓腹侧面（VMS）是一个在高碳酸血症期间已知会发挥呼吸刺激作用的区域。多项研究表明其参与了由缺氧引起的呼吸节律的中枢抑制。我们研究了从新生大鼠分离的脑干 - 脊髓标本，这些标本短暂地用极低氧的培养基灌注，导致可逆性呼吸抑制，以表征VMS在缺氧呼吸适应中的参与情况。在存在0.8 mM Ca²⁺的情况下，极低氧培养基诱导整个VMS中c - fos表达增加。0.2 mM Ca²⁺ - 1.6 mM Mg²⁺对突触传递的减少和呼吸驱动的阻断消除了内侧VMS（在锥体束外侧边缘）中的c - fos表达，但在面周后梯形核/旁面神经呼吸组（RTN/pFRG）VMS中未消除，这表明存在面周RTN/pFRG缺氧感应神经元。在存在Ca²⁺（0.8 mM）的情况下，损伤实验表明，至少在新生大鼠中，面周RTN/pFRG VMS在外侧VMS（在面神经核腹外侧部分下方）和中间VMS（在面神经核腹内侧部分下方）之间存在生理差异。外侧VMS损伤主要对应于pFRG最靠前的部分，产生了缺氧诱导的刺激，而中间VMS损伤对应于RTN的主要部分，消除了缺氧兴奋。这可能涉及通过内侧VMS的中继，内侧VMS被认为是锥体旁组。
