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

Abstract

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 (O₂)-induced learning and poisoning use the same or distinct cellular pathways. Purpose: We hypothesized that O₂-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) O₂, 1.4 ATA O₂, and 2.8 ATA O₂. 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) O₂ exposure did not affect CFFF and HR. Medium hyperbaric O₂ exposure (1.4 ATA) decreased CFFF but HR remained unchanged. High hyperbaric O₂ 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 O₂ on neuronal excitability measured by CFFF in young healthy men was dose dependent: 0.7 ATA O₂ did not affect CFFF; CFFF were significantly jeopardized at 1.4 ATA O₂, while CFFF recovered at 2.8 ATA. With 2.8 ATA O₂, the CFFF and oxygen poisoning transduction pathways seemed to be intertwined.

Keywords:

• Neuronal excitability
• Hyperbaric oxygen
• Normobaric oxygen
• Critical flicker fusion frequency
• Oxygen poisoning

We acknowledge Costantino Balestra (DAN Europe) for supporting this study.

ORCID

Jacek Kot http://orcid.org/0000-0001-5604-8407

Pawel Winklewski http://orcid.org/0000-0002-1671-2163

Additional information

Funding

The study was conducted as a part of the PHYPODE Marie Curie Initial Training Networks (FP7-PEOPLE-2010-ITN) and received funding from the People Programme (Marie Curie Actions) of the European Union’s Seventh Framework Programme FRP/2007-2013/ under the Research Executive Agency grant agreement [grant number 264816].