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

BackgroundPropofol, 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-B & ouml;tzinger complex (preB & ouml;tC), though the precise mechanisms are not well understood. In this study, we classify glutamatergic neurons in the brainstem preB & ouml;tC 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.MethodsWe first employed electrophysiological techniques to classify glutamatergic neurons within the preB & ouml;tC 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.ResultsWe 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 mu M and 10 mu M shortened the latency period of Type-1 glutamatergic neurons but did not affect the latency period of Type-2 glutamatergic neurons.ConclusionOur study focuses on the glutamatergic neurons in the preB & ouml;tC 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 preB & ouml;tC. These findings contribute to understanding the cellular basis of propofol-induced respiratory depression.