1953

Nathan Kline tests reserpine on patients at Rockland State Hospital (NY) and was soon promoting it as an “effective sedative for use in mental hospitals” (Valenstein, 69; Healy, I, 59-70; Healy, II, 104-05). At symposium at Ciba headquarters in Summit, NJ in 1953, Yonkman first uses the term “tranquilizer” to characterize mixture of sedation and well-being produced by reserpine (Healy, I,103-04). In 1955, Steve Brodie and colleagues at NIH reported that reserpine reduced the level of brain serotonin (I, 70 II, 106). Amine neurotransmitters are stored in small protective pouches, the synaptic vesicles, located at terminal endings; neurons adjacent to the synapse. Reserpine causes the biogenic amines to leak out of the vesicles, thus stimulating neighboring neurons and leading to the initial excitatory effect of the drug (I, 71). “Throughout the 1950s, reserpine was far more frequently mentioned in the scientific literature than chlorpromazine” (II, 106).