Abstract

The effect of the carbonic anhydrase inhibitor Acetazolamide on the response of worker honeybee antennal CO2-receptors to CO2 and N2O was tested by extracellular recordings of spike activity from single cells. 1. Within 15 minutes after oral application of Acetazolamide the spike frequency of the response to test stimuli of constant CO2-concentration decreases to a lower but constant value. 2. Stimulus-response curves measured after subsequent applications of increasing Acetazolamide doses are shifted towards higher CO2-concentrations to an extent which is related to the Acetazolamide dose. 3. The effect of Acetazolamide on the phasic peak of the CO2-response is more pronounced than the effect on the plateau. 4. The response to N2O, which is antagonistic to the CO2-response, is not affected by the presence of Acetazolamide. 5. When a CO2-stimulus of high concentration is applied in the presence of a very high Acetazolamide concentration, a response is observed which indicates that CO2 also can cause an effect of the same kind as N2O. 6. It is concluded that the effect of Acetazolamide results from its inhibitory action on a molecular acceptor with a CO2-binding site similar to that in carbonic anhydrase. 7. It is suggested that the responses to N2O and Xe and also the antagonistic component of the response to high concentrations of CO2 result from the action of those gases on a secondary step in the chain of sensory transduction.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.