Olfactory receptor response to CO2 in bullfrogs

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.

The neuronal correlates of intranasal trigeminal function—an ALE meta-analysis of human functional brain imaging data

“…Evidence supporting the first hypothesis, the existence of olfactory receptors responsive to CO 2 , comes from a range of animal models, including bullfrogs (Coates and Ballam, 1990; Sakakibara, 1978), tegu lizards (Coates and Ballam, 1987), reptiles (Coates and Ballam, 1989), and mice (Hu et al, 2007). Furthermore it is possible that olfactory brain areas are activated during the perception of trigeminal CO 2 stimuli via trigeminal ganglion cells with sensory endings in the nasal epithelium that also send branches into the olfactory bulb and the spinal trigeminal complex which were discovered by Schaefer and colleagues (2002).…”

Afferent input modulates the chronic hypercapnia-induced increase in respiratory-related central pH/CO2 chemosensitivity in the cane toad (Bufo marinus)

“…Stimulation of these chemoreceptors during acute hypoxia and hypercapnia leads to an increase in breathing (West et al, 1987;Smatresk and Smits, 1991). CO 2 -sensitive olfactory chemoreceptors, located in the nasal epithelium (Coates and Ballam, 1990;Coates, 2001), inhibit breathing when stimulated by physiologically relevant levels of inspired CO 2 (Sakakibara, 1978;Coates, 2001;Kinkead and Milsom, 1996;Milsom et al, 2004). Pulmonary stretch receptors (PSR), located in the walls of the lungs, monitor both the breath-bybreath changes in lung volume during inspiration and expiration as well as the degree of lung inflation during periods of apnea.…”

Carbon dioxide‐sensitive superior laryngeal nerve afferents in the anaesthetized cat

“…It is well established that CO2 alters the discharge of airway sensory receptors (Mustafa & Purves, 1972;Bartlett & Sant'Ambrogio, 1976;Coates & Ballam, 1990). In the first study of superior laryngeal nerve (SLN) mechanoreceptor responses to C02, Boushey, Richardson, Widdicombe & Wise (1974) described excitatory and inhibitory effects in response to blowing 5 and 10% CO2 in 02 over the exposed mucosa of the larynx, opened by a ventral mid-line incision in anaesthetized, paralysed cats.…”