Melega_1984_Proc.Natl.Acad.Sci.U.S.A_81_6535

Treatment of PC12 cells with AH5183 at concentrations of 40 nM to 40 microM inhibited the loading of newly synthesized acetylcholine into storage vesicles, but it had little effect on choline uptake, acetylcholine synthesis, or the vesicular content of previously loaded acetylcholine. AH5183 at 4 microM inhibited the Ba2+-evoked release of newly synthesized acetylcholine but not of older stores of acetylcholine. These data indicate that the vesicles are the source of the acetylcholine released from stimulated cells. AH5183 had little effect on the vesicular loading of dopamine and on the evoked release of dopamine, but at concentrations of 4-40 microM it did inhibit dopamine uptake by the cells.