Ritucci N A, Dean J B, Putnam R W
Department of Physiology and Biophysics, Wright State University, Dayton, Ohio 45435, USA.
Am J Physiol. 1997 Jul;273(1 Pt 2):R433-41. doi: 10.1152/ajpregu.1997.273.1.R433.
We investigated whether neurons in two chemosensitive areas of the medulla oblongata [nucleus of the solitary tract (NTS) and ventrolateral medulla (VLM)] respond to hypercapnia differently than neurons in two nonchemosensitive areas of the medulla oblongata [inferior olive (IO) and hypoglossal nucleus (Hyp)]. Medullary brain slices from preweanling Sprague-Dawley rats were loaded with 2',7'-bis(carboxyethyl)-5(6)-carboxyfluorescein, and intracellular pH (pHi) was followed in individual neurons at 37 degrees C with the use of a fluorescence imaging system. Most neurons from the NTS and VLM did not exhibit pHi recovery when CO2 was increased from 5 to 10% at constant extracellular HCO3- concentration [extracellular pH (pHo) decreased approximately 0.3 pH unit] (hypercapnic acidosis). However, when CO2 was increased from 5 to 10% at constant pHo (isohydric hypercapnia), pHi recovery was seen. In contrast, all neurons from the IO and Hyp exhibited pHi recovery during hypercapnic acidosis. All pHi recovery in the four areas studied was inhibited by 1 mM amiloride and unaffected by 0.5 mM 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid. These data indicate that 1) pHi regulation differs between neurons in chemosensitive (NTS and VLM) and nonchemosensitive (IO and Hyp) areas of the medulla, 2) pHi recovery is due solely to Na+/H+ exchange in all four areas, and 3) Na+/H+ exchange is more sensitive to inhibition by extracellular acidosis in NTS and VLM neurons than in IO and Hyp neurons.
我们研究了延髓两个化学敏感区域[孤束核（NTS）和延髓腹外侧区（VLM）]中的神经元对高碳酸血症的反应是否与延髓两个非化学敏感区域[下橄榄核（IO）和舌下神经核（Hyp）]中的神经元不同。将来自断奶前Sprague-Dawley大鼠的延髓脑片加载2'，7'-双（羧乙基）-5（6）-羧基荧光素，并使用荧光成像系统在37℃下跟踪单个神经元的细胞内pH（pHi）。当在细胞外HCO3-浓度恒定的情况下将CO2从5%增加到10%[细胞外pH（pHo）降低约0.3个pH单位]（高碳酸性酸中毒）时，NTS和VLM的大多数神经元未表现出pHi恢复。然而，当在pHo恒定的情况下将CO2从5%增加到10%（等氢离子高碳酸血症）时，观察到pHi恢复。相比之下，IO和Hyp的所有神经元在高碳酸性酸中毒期间均表现出pHi恢复。在所研究的四个区域中，所有pHi恢复均受到1 mM氨氯吡咪的抑制，且不受0.5 mM 4,4'-二异硫氰基芪-2,2'-二磺酸的影响。这些数据表明：1）延髓化学敏感（NTS和VLM）和非化学敏感（IO和Hyp）区域的神经元之间pHi调节不同；2）在所有四个区域中，pHi恢复仅归因于Na+/H+交换；3）与IO和Hyp神经元相比，NTS和VLM神经元中的Na+/H+交换对细胞外酸中毒抑制更敏感。
