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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We tested the hypothesis that decreasing the control level of O2 from 95% to 40% reduces tissue partial pressure of oxygen (pO2), decreases extracellular nitric oxide (NO) and decreases intracellular superoxide (O2) 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% O2 were comparable to recordings made in 95% O2 in 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 pO2 was threefold lower in 40% O2 versus 95% O2. Likewise, extracellular NO and intracellular O2 were lower in 40% versus 95% O2. 67% of neurons maintained in 40% O2 control were stimulated by hyperoxia (95% O2) compared to 81% of neurons maintained in 95% O2 that were stimulated during hyperoxic reoxygenation following acute exposure to 0–40% O2. cSC slices maintained in 40% O2 exhibited 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 CO2 chemosensitive. 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 CO2 chemosensitivity (e.g., increased expression of CO2-inhibition) compared to sustained hyperoxia (85–95% O2).