Stellate ganglia (SG) are sympathetic autonomic ganglia that provide sympathetic nerve inputs into the heart and may predispose the myocardial conducting system to atrial and ventricular arrhythmias. In recent years studies have shown a correlation between Parkinson’s disease (PD) and cardiac disease which imply autonomic dysregulation in PD. A30P point mutation of alpha-synuclein is a well-established risk factor in PD; A30P mutant alpha-synuclein mouse recapitulates systemically presenting alpha-synucleinopathy. We aim to investigate histological and electrophysiological properties of the stellate ganglia in light of alpha-synucleinopathy in PD.

Firstly, we here demonstrate that A30P mutant alpha-synuclein is expressed in the sympathetic adrenergic cells in stellate ganglia in the PD animal model. This finding contradicts Braak’s hypothesis that canonically regards the vagal nerve as the primary gateway of alpha-synuclein propagation. Secondly, we have developed a technique to patch stellate ganglionic tissue for electrophysiological examination and we here present sodium and potassium channel properties of murine stellate ganglia.

To investigate further, we aim to study the electrophysiology of stellate ganglia in A30P mutant mice, which will help explain the increased risk of cardiac dysautonomia in PD.