Avian intrapulmonary chemoreceptor discharge rate is increased by anion exchange blocker ‘DIDS’

Avian intrapulmonary chemoreceptors (IPC) are neurons that sense lung P_CO2 and provide phasic feedback for the control of breathing in birds. To try to understand mechanisms of CO₂ transduction and intracellular pH regulation in IPC, the anion exchange inhibitor 4,4′-diisothiocyanostilbene-2,2′-disulfonic acid (DIDS) was used to block transmembrane Cl⁻/HCO₃⁻ transport. Single-unit IPC discharge rates were measured at steady intrapulmonary CO₂ levels and during step changes in CO₂ in 15 anesthetized, unidirectionally ventilated adult mallard ducks (Anas platyrhynchos). Measurements were repeated after giving 50, 100 and 200 μmol/kg cumulative i.v. dosages of DIDS. Mean IPC discharge rates at steady (tonic) P_CO2 levels were significantly increased by 100 and 200 μmol/kg DIDS, but not by 50 μmol/kg DIDS. Mean dynamic (phasic) IPC responses to CO₂ steps were not significantly affected by DIDS. Results indicate that the DIDS-sensitive Cl⁻/HCO₃⁻ membrane exchanger is involved with tonic CO₂ signal transduction in IPC. However, because some individual IPC were unaffected by DIDS, yet still altered their discharge rate with CO₂, additional mechanisms besides the Cl⁻/HCO₃⁻ exchange are probably required for CO₂ chemotransduction in IPC.