Anti-panic medication and catecholaminergic systems
Tricyclic antidepressants and monoamine oxidase inhibitors are often an efficacious treatment of panic disorder. This effect is seen only after long-term treatment with these drugs. After the administration of first doses, tricyclics actually exacerbate the panic symptoms, probably as they increase the synaptic availability of norepinephrine in the brain as well as in the periphery. Antidepressant medication is thus not only efficacious in both depression and PD, but also produces anxiogenic as well as anxiolytic effects depending on the phase of treatment. Several studies carried out on patients with major depression and PD patients provided evidence that the antidepressants normalize a dysregulation of the noradrenergic system that is present in both conditions (Klein & Fink, 1962; Sargant & Dally, 1962; Nutt, 1989; Johnston et al., 1988; Nutt & Glue, 1989). Tricyclic antidepressants and MAO inhibitors also proved to be potent blockers of lactate-induced panic attacks (Rifkin et al., 1981, Liebowitz et al., 1984). Alfa2-adrenoreceptor agonist clonidine is a drug with anti-panic properties that also decreases the firing rate of locus ceruleus by acting on the inhibitory autoreceptors (Liebowitz et al., 1981, Hoehn-Saric et al., 1981). Nutt (1986) studied the effects of clonidine on healthy subjects and PD patients. He demonstrated that the patients treated with clonidine had significantly greater decreases in plasma MHPG levels than healthy controls. In another study, Nutt (1989) challenged PD patients and healthy controls with an infusion of clonidine. Compared to controls, the PD patients had a significant drop in plasma MHPG as well as a significant decrease of anxiety as compared to their baseline levels. Together, these results could imply that in PD, the inhibitory autoreceptors are hypersensitive.