Electrophysiological effects of propofol on glutamatergic neurons in mice Pre- Bötzinger Complex

Background Propofol, a commonly used intravenous anesthetic, can lead to a range of respiratory adverse events, particularly varying degrees of respiratory depression, which is closely linked to patient safety. However, the mechanisms underlying these respiratory adverse events caused by propofol remain unclear. In mammals, the initiation of breathing relies on rhythmic activity of glutamatergic neurons within the pre-Bötzinger complex in the lower brainstem. Previous studies have suggested that propofol-induced respiratory depression might be associated with glutamatergic neurons in the pre-Bötzinger complex, though the precise mechanisms are not well understood. This study aims to investigate the effects of propofol on the electrophysiological properties of glutamatergic neurons in the pre-Bötzinger complex. Methods We first employed electrophysiological techniques to classify glutamatergic neurons within the pre-Bötzinger complex. Based on this classification, we then continuously infused different concentrations of propofol to observe its effects on the electrophysiological properties of these various types of glutamatergic neurons. Results We found that Type 1 neurons exhibited a longer latency in excitation, while Type 2 neurons did not show this delayed excitation. Furthermore, continuous infusion of propofol at concentrations of 5 µM and 10 µM was observed to shorten the latency period of Type 1 glutamatergic neurons, but did not affect the latency period of Type 2 glutamatergic neurons. Conclusion Our study introduces a novel method for classifying glutamatergic neurons and reveals how propofol affects the activity of different types of glutamatergic neurons within the pre-Bötzinger complex. These findings contribute to understanding the cellular basis of propofol-induced respiratory depression.