{"title":"Avian intrapulmonary chemoreceptor discharge rate is increased by anion exchange blocker ‘DIDS’","authors":"J.M Shoemaker , S.C Hempleman","doi":"10.1016/S0034-5687(01)00273-0","DOIUrl":null,"url":null,"abstract":"<div><p>Avian intrapulmonary chemoreceptors (IPC) are neurons that sense lung P<sub>CO<sub>2</sub></sub> and provide phasic feedback for the control of breathing in birds. To try to understand mechanisms of CO<sub>2</sub> 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<sup>−</sup>/HCO<sub>3</sub><sup>−</sup> transport. Single-unit IPC discharge rates were measured at steady intrapulmonary CO<sub>2</sub> levels and during step changes in CO<sub>2</sub> in 15 anesthetized, unidirectionally ventilated adult mallard ducks (<em>Anas platyrhynchos</em>). Measurements were repeated after giving 50, 100 and 200 μmol/kg cumulative <em>i.v.</em> dosages of DIDS. Mean IPC discharge rates at steady (tonic) P<sub>CO<sub>2</sub></sub> levels were significantly increased by 100 and 200 μmol/kg DIDS, but not by 50 μmol/kg DIDS. Mean dynamic (phasic) IPC responses to CO<sub>2</sub> steps were not significantly affected by DIDS. Results indicate that the DIDS-sensitive Cl<sup>−</sup>/HCO<sub>3</sub><sup>−</sup> membrane exchanger is involved with tonic CO<sub>2</sub> signal transduction in IPC. However, because some individual IPC were unaffected by DIDS, yet still altered their discharge rate with CO<sub>2</sub>, additional mechanisms besides the Cl<sup>−</sup>/HCO<sub>3</sub><sup>−</sup> exchange are probably required for CO<sub>2</sub> chemotransduction in IPC.</p></div>","PeriodicalId":20976,"journal":{"name":"Respiration physiology","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2001-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0034-5687(01)00273-0","citationCount":"17","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Respiration physiology","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0034568701002730","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 17
Abstract
Avian intrapulmonary chemoreceptors (IPC) are neurons that sense lung PCO2 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) PCO2 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.