Abstract

AbstractCalmodulin (CaM) isolated from freshwater mussel gill has been shown to be present in fractions derived solely from epithelial cells of whole gill tissue. This CaM has been used to activate bovine brain phosphodiesterase (PDE) and the dose dependence of trifluoperazine‐dihydrochloride (TFP)‐mediated inhibition of activation has been investigated. The dose‐response curve yields an apparent K1 of 20 μM and suggests that at low concentration (up to 40 μM) TFP inhibits PDE activity in the presence of Ca2+, not by direct action on the enzyme, but by a shunt that negates the effect of mussel gill CaM.To determine whether CaM is physiologically significant for ciliary activity in the mussel gill, the effect of TFP upon the Ca2+‐dependent ciliary arrest response of the lateral (L) cells of the gill has been examined. Detergent‐treated permeabilized epithelial L cell models are scored for ciliary activity after transfer to reactivation solutions that vary in their free Ca2+ and TFP content. At 10−5 M free Ca2+ (pCa 5), maximum recovery from arrest is observed for TFP concentrations in the range of 25 to 30 μM. TFP‐mediated recovery from arrest is never complete, suggesting that in the presence of sufficient Ca2+ the drug irreversibly damages a certain fraction of axonemes. At pCa 7 the cilia reactivate and 25–30.

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