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J Appl Physiol 94: 1204-1212, 2003. First published November 15, 2002; doi:10.1152/japplphysiol.00558.2002
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Vol. 94, Issue 3, 1204-1212, March 2003

Central CO2 chemoreception in developing bullfrogs: anomalous response to acetazolamide

Barbara E. Taylor1, Michael B. Harris1, E. Lee Coates2, Matthew J. Gdovin3, and J. C. Leiter1

1 Department of Physiology, Dartmouth Medical School, Lebanon, New Hampshire 03756-0001; 2 Department of Biology, Allegheny College, Meadville, Pennsylvania 16335; and 3 Biology Department, University of Texas at San Antonio, San Antonio, Texas 78249

Central CO2 chemoreception and the role of carbonic anhydrase were assessed in brain stems from Rana catesbeiana tadpoles and frogs. Buccal and lung rhythms were recorded from cranial nerve VII and spinal nerve II during normocapnia and hypercapnia before and after treatment with 25 µM acetazolamide. The lung response to acetazolamide mimicked the hypercapnic response in early-stage and midstage metamorphic tadpoles and frogs. In late-stage tadpoles, acetazolamide actually inhibited hypercapnic responses. Acetazolamide and hypercapnia decreased the buccal frequency but had no effect on the buccal duty cycle. Carbonic anhydrase activity was present in the brain stem in every developmental stage. Thus more frequent lung ventilation and concomitantly less frequent buccal ventilation comprised the hypercapnic response, but the response to acetazolamide was not consistent during metamorphosis. Therefore, acetazolamide is not a useful tool for central CO2 chemoreceptor studies in this species. The reversal of the effect of acetazolamide in late-stage metamorphosis may reflect reorganization of central chemosensory processes during the final transition from aquatic to aerial respiration.

isolated brain stem preparation; carbonic anhydrase; acetazolamide; hypercapnia


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