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Much of the research on hallucinogenic drugs such as LSD has focused on the neurotransmitter serotonin, a chemical that when released from a presynaptic serotonin-secreting neuron causes the transmission of a nerve impulse across a synapse to an adjacent postsynaptic, or target, neuron. There are two major reasons for this emphasis. First, it was discovered early on that many of the major hallucinogens have a molecular structure similar to that of serotonin. In addition, animal studies of brain neurochemistry following administration of hallucinogens invariably reported changes in serotonin levels. Early investigators correctly reasoned that the structural similarity to the serotonin molecule might imply that LSDs effects are brought about by an action on the neurotransmission of serotonin in the brain. Unfortunately, the level of technical expertise in the field of brain research was such that this hypothesis had to be tested on peripheral tissue . Two different groups of scientists reported that LSD powerfully blockaded serotonins action. Their conclusions were quickly challenged, however. We now know that the action of a drug at one site in the body does not necessarily correspond to the drugs action at another site, especially when one site is in the brain and the other is not. By the 1960s, technical advances permitted the direct testing of the hypothesis that LSD and related hallucinogens act by directly suppressing the activity of serotonin-secreting neurons themselvesthe so-called presynaptic hypothesis. Researchers reasoned that if the hallucinogenic drugs act by suppressing the activity of serotonin-secreting neurons, then drugs administered after these neurons had been destroyed should have no effect on behavior, because the system would already be maximally suppressed. Contrary to their expectations, neuron destruction enhanced the effect of LSD and related hallucinogens on behavior. Thus, hallucinogenic drugs apparently do not act directly on serotonin-secreting neurons. | 
