No abstract

In vivo electrophysiological recordings of olfactory receptor cells of the bullfrog (Rana catesbeiana) exhibit a receptor response to CO2 concentrations as low as 0.5%. The amplitude of the electroolfactogram (EOG) increased with an increase in the CO2 concentration delivered to the olfactory epithelium. Likewise, there was a significant increase in the decay time (time from 90 to 10% peak EOG amplitude) with an increase in CO2. The EOG rise time (time from 10 to 90% peak EOG amplitude) and the EOG response latency (time from beginning of CO2 pulse to beginning of EOG response) significantly decreased, whereas the plateau time (time from 90% rising phase to 90% falling phase of the peak EOG amplitude) was not significantly altered by an increase in CO2. These results indicate that low concentrations of CO2, below normal end expiratory CO2 concentrations, stimulate olfactory receptor cells. These results support our proposal that the ventilatory depression observed in response to upper airway CO2 in reptiles and amphibians is mediated by CO2-sensitive olfactory receptor cells.

No abstract

The ventilatory response of the garter snake, Thamnophis sirtalis, to 2% CO2 delivered to the upper airways (UA) was measured before and after the olfactory or vomeronasal nerves were transected. The UA (nasal cavities and mouth) were isolated from the gas source inspired into the lungs by inserting an endotracheal T tube into the glottis. CO2 was administered to the UA via a head chamber. The primary ventilatory response to UA CO2 was a significant decrease in ventilatory frequency (f) and minute ventilation. The decrease in f was caused by a significant increase in the pause duration. Tidal volume, expiratory duration, and inspiratory duration were not altered with UA CO2. The f response to UA CO2 was abolished with olfactory nerve transection, whereas vomeronasal nerve transection significantly increased the magnitude of the f depression. These results indicate that CO2-sensitive receptors are located in the nasal epithelium and that the olfactory nerves must be intact for the UA CO2 f response to be observed. In addition, the vomeronasal system appears to modulate the ventilatory response to UA CO2.

Awake upright White Leghorn roosters (Gallus domesticus) were unidirectionally ventilated. Electromyographic activity from inspiratory and expiratory muscles was recorded to demarcate inspiration and expiration. During inspiration, the rate of inflation of the air sac system was varied while the CO2 concentration of the gas passing through the lungs was maintained constant. Inspiratory duration was inversely related to the rate of inflation, producing an inspiratory volume-time threshold (VT) curve with a negative slope. When the CO2 concentration was increased in the lungs, the inspiratory VT curve shifted to the right with a concurrent increase in slope. If the rate of deflation was varied during expiration, it was found that expiratory duration was inversely related to the rate of deflation, producing an expiratory VT curve with a positive slope. Increasing the CO2 concentration shifted the curve to the left with an increased slope. These results indicate that inspiratory and expiratory phase durations are a function of both mechanical and chemical feedback.