Fig. 11.

Hypoxia induces a barrage of spiking in vitro. A: application of 300 μM sodium cyanide (NaCN), a pharmacological analog of hypoxia, led to increased spiking in an individual pBC inspiratory cell recorded in current clamp (top) and increased network activity measured as hypoglossal nerve (XIIn) rootlet discharge (bottom) in a brain stem slice preparation. At the peak of the stimulation, phasic, coordinated drive is abolished. B: firing pattern of pBC cell before (left) and after (right) NaCN challenge. The depolarization and increased spiking that occur in response to the hypoxic perturbation in vitro are qualitatively similar to the responses observed in our closed-loop model. C: summary data from 9 experiments showing burst duration (top) and frequency (bottom) changes for baseline, NaCN treatment, hypoxia treatment, and recovery (n = 9, *P < 0.05 ANOVA, Tukey’s least significant difference as post hoc test, baseline vs. hypoxia or NaCN; error bars are SE). NaCN and hypoxia challenges do not result in statistically significantly different responses and produce an equivalent perturbation of the breathing rhythm in our in vitro slice preparations.