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KCC and NKCC activity affect spike frequency adaptation in CO 2 ‐sensitive avian intrapulmonary chemoreceptors (1092.3)
Author(s) -
Meehan Shane,
Bassett Peter,
Lonjaret JeanGuillaume,
Hempleman Steve,
Sheridan Krystal
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.1092.3
Subject(s) - tonic (physiology) , cotransporter , chemistry , endocrinology , medicine , chemoreceptor , furosemide , biophysics , biology , sodium , receptor , biochemistry , organic chemistry
IPC are respiratory chemoreceptors that exhibit SFA, have phasic and tonic CO2 sensitivity, and help control breathing in birds. In IPC, large changes in PCO2, pHi, and [HCO3]i occur with each breath. Here we test the hypothesis that Cl‐ transmembrane flux may be involved in IPC CO2 transduction to balance intracellular [HCO3‐] changes. Furosemide (FU), an equipotent inhibitor of both K+ ‐Cl‐ cotransport (KCC), which allows for Cl‐ efflux driven by the K+ gradient, and Na+ ‐K+ ‐2Cl‐ cotransport (NKCC), which allows for Cl‐ influx driven by the Na+ gradient, was given to anesthetized Anas platyrhynchos (N=6) while recording single‐unit IPC. FU progressively reduced SFA at 10‐40 mg/kg (p蠄0.0001). In contrast, tonic IPC discharge was decreased at low FU doses (0.5‐5 mg/kg, p蠄0.0001) but increased at higher dosages (10‐40 mg/kg, p蠄0.0001). Results suggest that IPC SFA and tonic CO2 sensitivity are influenced by KCC and/or NKCC, presumably by reducing ability of the cell to produce Cl‐ counter movements required by phasic [HCO3‐] changes. Grant Funding Source : Supported by NIH R15 HL087269‐02