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Trazodone was first synthesized in Italy about three decades ago, and clinical studies began in the United States in 1978. Trazodone was different from the conventional antidepressants that were available at that time in several ways. It was the first triazolopyridine derivative to be developed as an antidepressant. In addition, it was developed as an outgrowth of a specific hypothesis (i.e., that depression is caused by an imbalance in the brain mechanisms responsible for the emotional integration of adverse unpleasant experiences). For this reason, new animal models that measured the response to noxious stimuli or situations were used as screening tests for developing the drug. In fact, trazodone is inactive in classic antidepressant screening tests, such as the reserpine model, the potentiation of yohimbine toxicity, and the behavioral despair/forced swim paradigm, yet it inhibits painful and conditioned emotional responses (Silvestrini 1980). Trazodone shares with the phenothiazines the ability to suppress self-stimulation behavior and amphetamine effects, and it produces substantial blockade of -adrenergic receptors. In sharp contrast to most other antidepressants available at the time of its development, trazodone showed minimal effects on muscarinic cholinergic receptors.

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FIGURE 19–1. Chemical structure of trazodone.

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