Normobaric hyperoxia (95% O₂) stimulates CO₂-sensitive and CO₂-insensitive neurons in the caudal solitary complex of rat medullary tissue slices maintained in 40% O₂.
Normobaric hyperoxia (95% O₂) stimulates CO₂-sensitive and CO₂-insensitive neurons in the caudal solitary complex of rat medullary tissue slices maintained in 40% O₂.
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常压%20高氧%20(95%%20O·)%20刺激%20CO·敏感%20和%20CO·不敏感%20神经元%20in%20the%20caudal%20solitary%20complex%20of%20rat%20medullary%20tissue%
DOI：
10.1016/j.neuroscience.2014.03.017
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发表时间：
2014
期刊：
影响因子：
3.3
通讯作者：
Dean,JB
中科院分区：
文献类型：
--
作者：
Matott,MP;Ciarlone,GE;Putnam,RW;Dean,JB
我们测试了以下假设：将O2的控制水平从95%降低到40%，降低组织氧分压（pO 2），降低细胞外一氧化氮（radical dotNO），降低细胞内超氧化物（radical dotO 2 −），同时保持切片（直径300-400 μm;新生大鼠P2-22; 34-37 °C）中尾孤束复合体（cSC）神经元的活力。我们还测试了常压高氧是cSC神经元（包括CO2兴奋神经元）的一般刺激物的假设。维持在40%O2中的cSC神经元的全细胞记录在持续时间和质量上与95%O2中的记录相当。在40%O2中，cSC神经元的自发放电率显著降低，但与95%O2中维持的cSC神经元的膜电位和输入电阻相似。组织pO 2在40% O2中比在95% O2中低3倍。同样，细胞外自由基dotNO和细胞内自由基dotO 2 −在40%与95% O2中较低。67%的神经元维持在40%O2控制高氧刺激（95%O2）相比，81%的神经元维持在95%O2刺激期间高氧复氧急性暴露于0- 40%O2。在40%O2条件下培养的cSC脑片显示出CO2化学敏感神经元，包括CO2兴奋神经元（31.5%）和CO2抑制神经元（31.5%）。同样，在85- 95%O2中观察到较高的CO2抑制神经元发生率和较低的CO2兴奋神经元发生率。82%的O2兴奋神经元也对CO2化学敏感，CO2兴奋神经元（86%）和CO2抑制神经元（84%）同样受到高氧刺激。我们的研究结果表明，慢性（小时）和急性（分钟）暴露于高氧刺激放电率在大多数cSC神经元，其中大部分也是CO2化学敏感。我们的研究结果支持这样的假设，即反复暴露于急性高氧和高氧再氧-组织pO 2的反复激增-激活CO2化学敏感神经元中的氧化还原和亚硝化信号机制，从而改变CO2化学敏感性的表达（例如，CO2抑制的表达增加）与持续高氧（85- 95%O2）相比。
We tested the hypothesis that decreasing the control level of O2from 95% to 40% reduces tissue partial pressure of oxygen (pO2), decreases extracellular nitric oxide (radical dotNO) and decreases intracellular superoxide (radical dotO2−) while maintaining viability in caudal solitary complex (cSC) neurons in slices (∼300–400 μm; neonatal rat P2–22; 34–37 °C). We also tested the hypothesis that normobaric hyperoxia is a general stimulant of cSC neurons, including CO2-excited neurons. Whole-cell recordings of cSC neurons maintained in 40% O2were comparable to recordings made in 95% O2in duration and quality. In 40% O2, cSC neurons had a significantly lower spontaneous firing rate but similar membrane potentials and input resistances as cSC neurons maintained in 95% O2. Tissue pO2was threefold lower in 40% O2versus 95% O2. Likewise, extracellularradical dotNO and intracellularradical dotO2−were lower in 40% versus 95% O2. 67% of neurons maintained in 40% O2control were stimulated by hyperoxia (95% O2) compared to 81% of neurons maintained in 95% O2that were stimulated during hyperoxic reoxygenation following acute exposure to 0–40% O2. cSC slices maintained in 40% O2exhibited CO2-chemosensitive neurons, including CO2-excited (31.5%) and a higher incidence of CO2-inhibited (31.5%) neurons than previously reported. Likewise, a higher incidence of CO2-inhibited and lower incidence of CO2-excited neurons were observed in 85–95% O2. 82% of O2-excited neurons were also CO2-chemosensitive; CO2-excited (86%) and CO2-inhibited neurons (84%) were equally stimulated by hyperoxia. Our findings demonstrate that chronic (hours) and acute (minutes) exposure to hyperoxia stimulates firing rate in the majority of cSC neurons, most of which are also CO2chemosensitive. Our findings support the hypothesis that recurring exposures to acute hyperoxia and hyperoxic reoxygenation—a repeating surge in tissue pO2—activate redox and nitrosative signaling mechanisms in CO2-chemosensitive neurons that alter expression of CO2chemosensitivity (e.g., increased expression of CO2-inhibition) compared to sustained hyperoxia (85–95% O2).