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“Neurochemical Evidence That Hallucinogenic Drugs Are 5=HT1C Receptor Agonists: What Next?”.
NIDA Research Monograph. 1994 Oct;146:203-213.
Behavioral, electrophysiological, and neurochemical evidence points to the serotonin2(5-HT2) receptor as an important site of action for hallucinogenic drugs (Glennon, this volume). Several years ago, the hypothesis was developed that hallucinogenic drugs might also be 5-HT1C receptor agonists. This hypothesis was based on the significant sequence homology in the deduced amino acid structure of the 5-HT2 and 5-HT1C receptors, their pharmacological similarities, and the evidence that both receptors are linked to the same signal transduction pathway: phosphoinositide hydrolysis. In the past 4 years, the author and colleagues at Vanderbilt University have accumulated compelling evidence in support of this hypothesis.
A more profound question remaining unanswered is the relative roles of the 5-HT2 and 5-HT1C receptors in the various actions of these drugs, in particular, hallucinations. Studies of this question are just beginning and are based on three strategies: a neurochemical effect important to hallucinations should be a common property of all hallucinogenic drugs; close structural analogs of hallucinogenic drugs that do not elicit hallucinations should also not elicit the neurochemical response; and tolerance should develop to the behavioral effects of hallucinogenic drugs. Results of these studies are summarized in this chapter.
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