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J Appl Physiol (November 15, 2002). doi:10.1152/japplphysiol.00558.2002
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Articles in PresS, published online ahead of print November 15, 2002
J Appl Physiol, 10.1152/jap.00558.2002
Submitted on June 26, 2002
Accepted on November 12, 2002

Central CO2 chemoreception in developing bullfrogs: Anomalous response to acetazolamide

Barbara E Taylor1*, Micheal B Harris1, E. L Coates2, Matthew J Gdovin3, and J. C Leiter1

1 Department of Physiology, Dartmouth Medical School, Lebanon, NH, USA
2 Department of Biology, Allegheny College, Meadeville, PA, USA
3 Department of Biology, University of Texas, San Antonio, San Antonio, TX, USA

* To whom correspondence should be addressed. E-mail: barbara.e.taylor{at}dartmouth.edu.

Central CO2 chemoreception and the role of carbonic anhydrase were assessed in brainstems 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 and mid-stage 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 brainstem 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.




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