Medullary CO2 chemoreceptor neuron identification by c-fos immunocytochemistry.
Medullary CO2 chemoreceptor neuron identification by c-fos immunocytochemistry.
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通过 c-fos 免疫细胞化学鉴定髓质 CO2 化学感受器神经元。
DOI：
10.1152/jappl.1992.73.1.96
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发表时间：
1992
影响因子：
3.3
通讯作者：
A. Basbaum
中科院分区：
文献类型：
--
作者：
M. Sato;J. Severinghaus;A. Basbaum
在寻找脑干中 CO2 化学感受器神经元的过程中，我们使用免疫细胞化学来监测五组 Sprague-Dawley 大鼠（294 +/- 20 g）暴露于 CO2 1 小时后神经元 c-fos 的表达，这是活性增加的标志物：五组空气呼吸对照，三组呼吸 10% CO2，三组呼吸 13% CO2，三组呼吸 15% CO2，三组呼吸 15% CO2 并接受治疗吗啡（皮下注射 10 毫克/千克）。暴露后，用戊巴比妥钠麻醉大鼠并用4％多聚甲醛进行心内灌注。取出脑干并冷冻保护，然后切割 50 微米冷冻切片并进行 fos 蛋白免疫染色。在腹侧髓质表面浅层 0.5 mm 处绘制脑干 fos 免疫反应性神经元并进行计数。 13% 至 15% CO2 在 321 +/- 146 个神经元/大鼠中诱发 fos 样免疫反应性 (FLI)。显着的 CO2 诱导标记仅限于表面 150 微米内：67% 的已识别细胞位于表面以下不到 50 微米，大于 90% 位于距中线 1.0 至 3.0 毫米之间，大约 60% 位于髓质的前半部。 13% 至 15% 的 CO2 也会在孤束核区域引起 FLI，但不会在其他髓质区域引起 FLI。吗啡（10 mg/kg sc）不会抑制腹侧髓质表面或孤束核中高CO2诱发的FLI，尽管它消除了兴奋和过度换气。我们建议，在高碳酸血症 1 小时后，可以通过大鼠中 c-fos 的表达来识别呼吸 CO2 化学感受器神经元。（摘要截断为 250 字）
In a search for CO2 chemoreceptor neurons in the brain stem, we used immunocytochemistry to monitor the expression of neuronal c-fos, a marker of increased activity, after 1 h of exposure to CO2 in five groups of Sprague-Dawley rats (294 +/- 20 g): five air breathing controls, three breathing 10% CO2, three breathing 13% CO2, three breathing 15% CO2, and three breathing 15% CO2 and treated with morphine (10 mg/kg sc). After exposure the rats were anesthetized with pentobarbital sodium and perfused intracardially with 4% paraformaldehyde. The brain stem was removed and cryoprotected, and then 50-microns frozen sections were cut and immunostained for the fos protein. Brain stem fos-immunoreactive neurons were plotted and counted in the superficial 0.5 mm of the ventral medullary surface. Thirteen to 15% CO2 evoked fos-like immunoreactivity (FLI) in 321 +/- 146 neurons/rat. Significant CO2-induced labeling was confined within the superficial 150 microns: 67% of identified cells were less than 50 microns below the surface, greater than 90% between 1.0 and 3.0 mm from the midline, and approximately 60% in the rostral half of the medulla. Thirteen to 15% CO2 also evoked FLI in the area of the nucleus tractus solitarius but not in other medullary regions. Morphine (10 mg/kg sc) did not suppress high CO2-evoked FLI in either the ventral medullary surface or the nucleus tractus solitarius, although it eliminated excitement and hyperventilation. We suggest that respiratory CO2 chemoreceptor neurons can be identified in rats by their expression of c-fos after 1 h of hypercapnia.(ABSTRACT TRUNCATED AT 250 WORDS)