1. Acetylcholine release evoked from nerve terminals in vivo or in vitro results in a subsequent activation of choline uptake. 2. The activation of choline transport is not due to any obligatory coupling with acetylcholine synthesis because incoming choline is diluted with endogenous choline. 3. The choline carrier demonstrates trans-activation, i.e. influx stimulates efflux and vice versa. Acetylcholine is a weak competitor for the choline binding site and is hardly transported. 4. The binding of acetylcholine without concomitant transport has the effect of immobilizing the carrier on the side of the high acetylcholine concentration inside the terminal so that it is not available for the transport of choline from the outside. When intraterminal acetylcholine concentration is reduced by the release process the immobilization of the carrier is relieved thus enabling it to return to the outside of the membrane and activate choline uptake. 5. The choline carrier has been solubilized and incorporated into an artificial membrane system (liposomes). In liposomes the carrier demonstrates saturability, inhibition by hemicholinium-3 and trans-activation. The choline transported is not acetylated nor does S-acetyl-CoA increase the rate. Influx is stimulated by Na+ on the outside and K+ on the inside.