Abstract

Ganglionated Plexus (GP) is a complex neural network composed by intrinsic cardiac autonomic nervous system (ANS) and is mainly located in fat pads around the antrum of the pulmonary veins (PVs). Recent studies demonstrated hyperactivity of GPs and atrial fibrillation (AF) formed a vicious cycle, to be specific, hyperactivity of the cardiac GPs facilitated the initiation and maintenance of AF and the activity of cardiac GPs increased as AF continued. In addition, research has confirmed that the Nav1.8 channel is highly expressed in GPs and is closely related to activity of GPs and the inducibility of AF. Nerve growth factor (NGF) is an important neurotrophic factor and the expression of NGF in GPs is up-regulated during AF over time, which could trigger the release of SP in the heart via TRPV1 signaling pathways. Besides, SP could rapidly increase the activity of the Nav1.8 channel, demonstrating the increment of Sensory nerve action potentials. Therefore, we hypothesized that up-regulated NGF during AF could increase the activity of GPs through TRPV1-SP-Nav1.8 channel pathways and contributes to stability of AF. If this hypothesis is proved to be correct, future studies based on this link may help to find new therapeutic targets for the treatment of AF.

Keywords: Ganglionated Plexus; Atrial fibrillation; Nerve growth factor; Nav1.8 channel; TRPV1 receptor