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Abstract: Bitter taste detection is very important for many species including flies, because it prevents the ingestion of toxic food. Although it has been known that flies have specific bitter-sensitive taste cells in their contact chemosensilla, the mechanism by which those cells transduce the chemical signal into electrical activity has remained elusive. In this study, we first confirmed that type D4 and D5 tarsal chemosensilla of the blowfly Phormia regina responded well to bitter substances. Then, recording impulses from type D4 chemosensilla, we examined the possibility that a G-protein-coupled inositol 1,4,5-trisphosphate (IP3)-dependent transduction cascade is of importance in the bitter-sensitive taste cells. We found that the response to bitter substances was depressed by specific inhibitors of G-protein, phospholipase C, or IP3 receptor in the tarsal taste receptor cells. These results suggest that G-proteins mediate the IP3 pathway in the transduction cascade in bitter-sensitive receptor cells. [Copyright &y& Elsevier]

Abstract: Intrapulmonary chemoreceptors (IPC) are carbon dioxide sensing neurons that innervate the lungs of birds, control breathing pattern, and are inhibited by halothane and intracellular acidosis. TASK and TREK are subfamilies of tandem-pore domain potassium leak channels, important in setting resting membrane potential, that are affected by volatile anesthetics and acidosis. We hypothesized that such channels might underlie signal transduction in IPC. We treated mallard ducks with four volatile anesthetics in increasing concentrations to test their effects on IPC discharge through single cell, extracellular recording from vagal fibers. Isoflurane inhalation attenuated IPC discharge only at 8.25% inspired (α =0.05). Halothane attenuated IPC discharge significantly (α =0.05) at all treatment levels. Chloroform at 3.8%, 5.6%, and 8.25% significantly attenuated IPC discharge (α =0.05). Ether at 1.9%, 2.9%, and 3.8% significantly attenuated IPC discharge (α =0.05), abolishing IPC discharge at 3.8% inspired. The pharmacological signature of IPC discharge attenuation suggests that IPC express tandem-pore domain leak channels similar to TREK channels, which are inhibited by intracellular acidosis. [Copyright &y& Elsevier]

Abstract: Data indicate that avian intrapulmonary chemoreceptors (IPC) transduce CO2 stimuli by sensing the products of CO2 hydration, [H+] and [HCO3 −]. The alphastat regulation hypothesis of physiological pH sensitivity suggests that proteins sense [H+] through changes in the ionization state of imidazole groups (alphaIm). To test whether imidazole is involved with IPC CO2 sensitivity, we administered diethyl pyrocarbonate (DEPC) intravenously while recording from IPC exposed to varying levels of inspired CO2. At physiological pH, DEPC converts pH sensitive imidazole groups to pH-insensitive N-carbethoxyhistidyl residues. Single cell extracellular neural recordings were made from vagal filaments in anesthetized, unidirectionally ventilated Anas platyrhynchos. Without DEPC, IPC discharge rate was inversely proportional to inspired CO2 with characteristic dynamic responses to rapid CO2 alterations (n =10). After DEPC treatment (≥15mM), mean sensitivity of IPC discharge to static inspired CO2 levels was decreased 75% (P <0.05), and mean peak dynamic IPC discharge rate was decreased 80% (P <0.05). Additionally, we tested whether DEPC might alter IPC discharge by binding imidazole groups in the enzyme carbonic anhydrase (CA), but we found no effect on CA catalytic rate. We conclude that DEPC inhibits IPC CO2 signal transduction by modifying imidazole groups on acid-sensitive proteins other than CA, possibly membrane acid–base exchangers or ion channels. These data support the alphastat regulation hypothesis in IPC CO2 respiratory chemoreception and suggests a more direct link between H+ and membrane excitability. [Copyright &y& Elsevier]