Calmodulin and the transmitter release at the neuromuscular junction. Contradictory results obtained with trifluoperazine.

Abstract

Calmodulin seems to be strongly involved in the process of transmitter release. By activating a specific proteinkinase system, calmodulin could initiate the phosphorylation of some axolemal or vesicular protein, thus triggering the exocytosis of the synaptic vesicles and the transmitter release. Under these conditions it was to be expected that a calmodulin blocking agent such as trifluoperazine, used in appropriate concentrations for this effect, should block the transmitter release. Contradictory results determined us to reexamine the question under extended experimental conditions. Our data suggest that calmodulin could both activate and block the transmitter release through probably different mechanisms.