Much of the research on hallucinogenic drugs such as LSD has focused on the neurotransmitt

er 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 LSD' s effects arc 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 or, peripheral tissue (tissue outside the brain). Two different groups of scientists reported than LSD powerfully blockaded serotonin' s 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 drug' s action at another site, especially when one site is in the brain and the other is not.

By the 1960' s technical advances permitted the direct testing of the hypothesis that LSD and related hallucinogens act by directly suppressing the activity of serotonin secreting neurons themselves—the so called presynaptic hypothesis. Researchers reasoned that if the hallucinogenic drags 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.

However, these and other available data do support an alternative hypothesis, that LSD and related drugs act directly at receptor sites on serotonin target neurons (the postsynaptic hypothesis). The fact that LSD elicits "serotonin syndrome", that is, causes the same kinds of behaviors as does the administration of serotonin in animals whose brains are depleted of serotonin indicates that LSD acts directly on serotonin receptors, rather than indirectly through the release of stores of serotonin. The enhanced effect of LSD reported after serotonin depletion could be due to a proliferation of serotonin receptor sites on serotonin target neurons. This phenomenon often follows neuron destruction or neurotransmitter depletion; the increase in the number of receptor sites appears to be a compensatory response to decreased input. Significantly, this hypothesis is supported by number of different laboratories

According to the passage, which of the following is one of the primary factors that led researchers studying hallucinogenic drugs to focus on serotonin？

A．The suppression of the activity of serotonin-secreting neurons by the administration of hallucinogens.

B．The observed similarities in the chemical structures of serotonin and hallucinogens.

C．The effects the administration of hallucinogens has on serotonin production in the human brain.

D．Serotonin-induced changes in the effects of hallucinogens on behavior.