The 130 years between Claude Bernard's demonstration that curare blocks neuromuscular transmission, but not nerve conduction or muscular contraction, and the cloning of receptor that binds the drug saw the emergence of neuropharmacology. Propelled by the staggering economic growth of the 19
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Century and public support, the number of scientists and scientific institutions expanded enormously. It became clear that excitable cells interact though one‐way junctions without cytoplasmic continuity: synapses. Drugs were discovered that block transmission at specific synapses or mimic the effects of nerve stimulation. Some thought that drugs bound to specific receptor sites, perhaps on arms of the huge molecule then believed to make up the protoplasm. The crucial step in elucidating the mechanism of transmission and revealing how the drugs act was Loewi's demonstration, in 1921, that stimulated nerves release a chemical that acts on the effector like nerve stimulation. Many concluded that synaptic transmission is chemical. Others argued that this could not be because transmission is so fast—it must be electrical. The argument was finally resolved in the 1950's when it was shown that the potential changes produced by presynaptic nerve stimulation reverse in sign at a set level of postsynaptic potential, demonstrating that the released transmitters open ion channels in the postsynaptic membrane. Transmission is fast because the transmitters bind, open an ion channel, and then are promptly released so the channel closes. These receptors are operated by the high local concentrations of transmitter produced by quanta1 release. Understanding how drugs work at synapses led to new drugs and advances in health care—a stunning record of achievement.