Our studies are intended to characterize the process of axoplasmic transport in nerve and to analyze the underlying mechanism. We found that axoplasmic transport requires a continued supply of metabolic energy as ATP. More recently we found that Ca2 ion is also required to maintain axoplasmic transport. Our present studies are directed to showing how Ca2 ion is regulated within the mammalian nerve fibers in relation to the transport mechanism. The Ca2 ion-regulatory mechanisms appear to be similar to those found in other cells. These include sequestration of Ca2 ion in the mitochondria and endoplasmic reticulum as well as to Ca2 ion binding protein (CaBP). Our studies appear to indicate that this CaBP we found in nerve is the same as or identical to calmodulin. This protein is being further investigated. Calmodulin is known to activate a number of enzymes including Ca2 ion-Mg2 ion-ATPase. We are showing in our studies of calmodulin obtained from nerve that it activates the Ca2 ion-Mg2ion-ATPase also obtained from nerve. We consider that the calmodulin is carried down in association with the transport filaments in our model of axoplasmic transport. The calmodulin activates the Ca2 ion-Mg2 ion-ATPase present on the side-arms of microtubules, the utilization of ATP in the process being a necessary part of the process by which the transport filaments are moved down within the fibers.