Abstract:

The physiological functions of visceral organs such as the heart are maintained within a healthy range by a variety of homeostatic mechanisms, including the actions of the sympathetic and parasympathetic nervous systems. However, one of the most common drivers of human disease is an imbalance in this autonomic system that is characterized by a pathological increase in sympathetic activity. How then do sympathetic neurons normally maintain their activity within a homeostatic range, and why is this regulation disrupted in hypertension and other disorders? In this work we use rat models and chemogenetic proteins to alter sympathetic activity and examine activity-dependent processes within the peripheral sympathetic ganglia. We find that that multiple plasticity mechanisms contribute to setting the level of sympathetic output and identify a role for sympathetic satellite glia in driving homeostatic plasticity in the sympathetic system.