Abstract
Alprazolam is a triazolobenzodiazepine which has been reported to be effective in the treatment of panic disorder (Ballenger et al., 1988). Although the mechanism of action of alprazolam in panic disorder has not been determined, the drug has been shown to decrease noradrenergic activity with the down-regulation of post-synaptic β-receptors in brain slices and animal studies (Charney et al., 1986). We have shown that alprazolam-treated patients with panic disorder and agoraphobia have an increase in the number of high-affinity platelet-tritiated imipramine binding sites which significantly correlates with improvement in symptoms of anxiety, depression and a decrease in the number of panic attacks (Pecknold et al., 1989). Platelet [3H]-imipramine binding sites appear to be associated with the uptake of serotonin (Langer et al., 1980). As it has been reported that serotonin may be involved in panic disorder (Pecknold, 1990) and that serotonergic agents such as clomipramine (Johnson et al., 1988) zimeldine (Evans et al., 1986) and fluvoxamine (den Boer and Westenberg, 1988) are effective in the treatment of panic disorder, the use of imipramine binding as a predictor of response to effective treatment is of major clinical interest.
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