Abstract

Panic attacks are associated with increased autonomic symptoms, suggesting increased β 2-adrenergic receptor (β 2AR) function in PD. Tricyclic antidepressants downregulate βAR function. Previous studies on βAR function in PD, however, are inconsistent. We recently found increased βAR coupling and density in neutrophils of symptomatic drug-free PD patients. This study evaluated βAR coupling to G s protein in 28 controls, 25 drug-free PD patients and 8 PD imipramine-treated patients. PD patients had significantly higher coupling and receptor density, particularly in the high-conformational state. Differences were more pronounced in patients with less depressive symptomatology. Treatment with imipramine was associated with decreased βAR coupling and density in the high-conformational state. Several βAR binding parameters were related to severity of anxiety symptoms and treatment outcome. Antidepressants downregulate βAR density and induce uncoupling from G s protein in PD. Future studies may investigate βAR coupling in relationship to treatment outcome and the role of βAR kinase in PD.

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