CARBONIC-ANHYDRASE AND CO2 CHEMORECEPTION IN THE PULMONATE SNAIL HELIX-ASPERSA

We have studied the effects of carbonic anhydrase inhibition on the hypercapnic ventilatory response of the pulmonate snail, Helix aspersa, in an isolated brain-pneumostome preparation. We found that the cell permeant carbonic anhydrase inhibitor, acetazolamide (ACTZ), increased pneumostomal opening and ventilation during normocapnia (2-3% CO2) and decreased the rate of pneumostomal response to step changes in CO2 (4.5%), but did not change the steady-state ventilatory response to elevated CO2 (4.5%) compared to the inactive ACTZ analogue, N-2-substituted 2-acetylamino-1,3,4-thiadiazole (Cl 13850). In contrast, the cell impermeant carbonic anhydrase inhibitor, quartenary ammonium sulfonilamide (QAS), had no effect on the pneumostomal response to CO2 compared to Cl 13850. Using Hansson's histochemical technique to stain for carbonic anhydrase activity, we identified a small number of neurons in the sub-esophageal ganglia that exhibited carbonic anhydrase activity. Some of these cells were in the region of CO2-sensitivity. In conclusion, carbonic anhydrase inhibition slows the ventilatory response to rapid changes in CO2, but does not affect the intrinsic ability of H. aspersa to respond to CO2. The ventilatory effects of carbonic anhydrase inhibition may be attributed to the intracellular actions of the carbonic anhydrase enzyme.