Trifluoperazine, a calmodulin antagonist, inhibits muscle cell fusion.

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Abstract
The effect of trifluoperazine (TFP), a calmodulin antagonist, was investigated on the fusion of chick skeletal myoblasts in culture. TFP inhibited myoblast fusion. This effect occurred at concentrations that were reported to inhibit Ca2+-calmodulin in vitro, and was reversed upon removal of TFP. Other calmodulin antagonists, including chlorpromazine, N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide (W7) and N-(6-aminohexyl)-1-naphthalenesulfonamide (W5), inhibited fusion at doses that corresponded closely to the antagonistic effects of these drugs on calmodulin. The expression of surface acetylcholine receptor, a characteristic aspect of msucle differentiation, was not impaired in TFP-arrested myoblasts. Myoblasts inhibited from fusion by 10 .mu.M TFP displayed impaired alignment. In the presence of the Ca2+ ionophore A23187 [calcimycin], the fusion block by 10 .mu.M TFP was partially reversed and myoblast alignment was restored. The presence and distribution of calmodulin in both prefusional myoblasts and fused muscle cells was established by immunofluorescence. An apparent redistribution of calmodulin staining that was temporally correlated with the onset of myoblast fusion was observed. A possible role for calmodulin in the regulation of myoblast fusion is suggested.