Ciliary inhibition and axonemal microtubule alterations in freshwater mussels.

A phenomenon associated with the genetic disease of cystic fibrosis (CF) is 
the presence of a serum factor that stops or discoordinates ciliary 
beating. This effect has been demonstrated by exposing freshwater mussel or 
oyster gill cilia, or rabbit tracheal cilia, to sera from homozygous 
or heterozygous cystic fibrosis subjects. Assay reproducibility is unsatisfactory, however, and 
the mechanism of the effect is not understood. Nor do we 
know why there may be considerable differences between the activity of 
tested heterozygotes and of homozygotes. Because the ciliary assay is capricious, 
there is a need to understand how ciliary beating is disturbed 
or stopped. Since microtubules are important in the mechanism of ciliary 
motion, they could conceivably show alterations during the response to inhibitory 
substances. There has been no ultrastructural study, however, of the effects 
of ciliary inhibition on the axonemal components. Therefore, this study was 
designed to examine ciliary structure during the different stages of ciliary 
inhibition. Rapid microtubular disappearance and reappearance occurs in the terminal cilia 
of the freshwater mussel Unio when exposure to CF serum causes 
a shock-stop reaction, and return to water allows resumption of normal 
ciliary beating. In contrast, a slow-stop reaction causes distortion of cilia, 
asynchronous beating, and ejection of cells from the distal gill filament, 
but ciliary axonemal structure is preserved. Slow-stopped cilia do not resume 
their beating in water. Saliva from reserpine-treated rats causes ciliary inhibition 
similar to that induced by CF serum. 