Effects of propofol on the electrophysiological properties of glutamatergic neurons in the ventrolateral medulla of mice.

BACKGROUND: Propofol, a commonly used intravenous anesthetic, is associated with various respiratory adverse events, most notably different degrees of respiratory depression, which pose significant concerns for patient safety. Respiration is a fundamental behavior, with the initiation of breathing in mammals dependent on neuronal activity in the lower brainstem. Previous studies have suggested that propofol-induced respiratory depression might be associated with glutamatergic neurons in the pre-Bötzinger complex (preBötC), though the precise mechanisms are not well understood. In this study, we classify glutamatergic neurons in the brainstem preBötC using whole-cell patch-clamp techniques and investigate the effects of propofol on the electrophysiological properties of these neurons. Our findings aim to shed light on the mechanisms of propofol-induced respiratory depression and provide new experimental insights. METHODS: We first employed electrophysiological techniques to classify glutamatergic neurons within the preBötC as Type-1 or Type-2. Following this classification, we applied varying concentrations of propofol through bath application to examine its effects on the electrophysiological properties of each type of glutamatergic neuron. RESULTS: We found that Type-1 neurons exhibited a longer latency in excitation, while Type-2 neurons did not show this delayed excitation. On this basis, we further observed that bath application of propofol at concentrations of 5 μM and 10 μM shortened the latency period of Type-1 glutamatergic neurons but did not affect the latency period of Type-2 glutamatergic neurons. CONCLUSION: Our study focuses on the glutamatergic neurons in the preBötC of adult mice. It introduces a novel method for classifying these neurons and reveals how propofol affects the activity of the two different types of glutamatergic neurons within the preBötC. These findings contribute to understanding the cellular basis of propofol-induced respiratory depression.