Particulate matter exposure decreased spiking response to depolarization and increased potassium current of cardiac vagal neurons in mice

Abstract

Epidemiologic studies show that exposure to fine particulate matter (PM2.5) increases the total daily cardiovascular mortality. W previously showed that 3 d of PM2.5 exposure (6 hr/d) in the form of iron‐soot reduced heart rate variability in mice. We further showed that PM2.5 exposure reduced neuronal responsiveness to excitation in cardiac vagal neurons in the nucleus ambiguus. Here, we tested the hypothesis that PM2.5 exposure‐induced increases in potassium currents contribute to the decreased neuronal excitability. Using patch‐clamp techniques, we determined the spiking response to depolarization and potassium currents in anatomically identified cardiac vagal neurons, retrogradely labeled with a fluorescent dye applied to the SA node. PM2.5 exposure decreased spiking responses of identified cardiac vagal neurons to depolarization in the presence of glutamatergic and GABAergic receptor antagonists (p < 0.05). PM exposure also increased the peak (by 24%) and stead state (by 17%) potassium currents. The data suggest that PM2.5 exposure‐induced increase in potassium channel conductance maybe one mechanism contributing to the decreased heart rate variability. (Support R01 ES012957)