Effect of oxygen on neuronal excitability measured by critical flicker fusion frequency is dose dependent

摘要

Introduction: Reactive oxygen species are involved in the functional changes necessary for synaptic plasticity, memory, and cognitive function. It is far from clear whether the increased excitability, and which forms of neuronal excitability, should be considered a part of the learning process or, rather, cellular manifestation of neuronal oxygen poisoning. It is yet to be elucidated whether oxygen (O-2)-induced learning and poisoning use the same or distinct cellular pathways. Purpose: We hypothesized that O-2-induced neuronal excitability might use the same or an intertwined signaling cascade as the poisoning cellular pathway. Method: Eighty-one healthy, young males, mean age 27.7 +/- 4.1 (SD) years, were exposed in the hyperbaric chamber to 0.7 atmosphere absolute (ATA) O-2, 1.4 ATA O-2, and 2.8 ATA O-2. The critical flicker fusion frequency (CFFF), oxyhemoglobin saturation (SiO2), and heart rate (HR) were measured before exposure, after 30 min of oxygen breathing while still at pressure and then after exposure. Results: Normobaric (0.7 ATA) O-2 exposure did not affect CFFF and HR. Medium hyperbaric O-2 exposure (1.4 ATA) decreased CFFF but HR remained unchanged. High hyperbaric O-2 exposure (2.8 ATA) increased CFFF and diminished HR. SiO2 was similar in all investigated groups. A correlation between CFFF, HR, and SiO2 was observed only at low oxygen (0.7 ATA). Conclusions: The effect of O-2 on neuronal excitability measured by CFFF in young healthy men was dose dependent: 0.7 ATA O-2 did not affect CFFF; CFFF were significantly jeopardized at 1.4 ATA O-2, while CFFF recovered at 2.8 ATA. With 2.8 ATA O-2, the CFFF and oxygen poisoning transduction pathways seemed to be intertwined.