Hyperbaric Oxygen Depolarizes Solitary Complex Neurons In Tissue Slices Rat Medulla Oblongata

Abstract

Hyperbaric oxygen (HBO₂)at 3 atmospheres absolute (ATA) pressure is toxic to the mammalian CNS due to excessive free radical production. No study has ever determined the effects of ≤3 ATA of O₂ on the membrane potential and firing rate of neurons in the mammalian brainstem. Likewise, no study has ever determined the effects of ≤3 ATA pressure per se on brainstem neurons. Accordingly, we initiated intracellular recordings at 1 .ATA in solitary complex neurons in slices (300 μ of rat caudal medulla oblongata that were maintained inside a 72 liter hyperbaric chamber. Helium, which is inert and without narcotic effect at moderate levels of hyperbaria, was used to hydro-statically compress the submerged brain slice to determine the effects of pressure per se. Tissue oxygen tension and extracellular pH were also measured during exposure to hyperbaric gases. Six of 19 neurons were affected by hyperburic helium; 5 cells were depolarized and 1 cell was hyperpolanzcd. Input resistance (R_m)either increased (n=1)or decreased (n 2) When control perfusatc (0.95 ATA O₂) was switched to perfusate saturated with 98%O₂ (balance CP₂, PH=7.3•7.4, pO₂ 23–34 ATA; 2–18 minutes of exposure) in a separate pressure vessel, 8 of 13 neurons were depolarized and 5 neurons were insensitive. In the 8 O-responsive neurons, R_m either increased (n 5). decreased (n 2) or was unchanged (n=⌋). Three of 8 neurons depolarized by HBOP₂ were also depolarized by hyperbaric helium, usually with an additional change in R_m We conclude that hydrostatic (helium) pressure and HBO₂ independently increase excitability in certain solitary complex neurons. We hypothesize that these responses contribute, in part, to neural events that either precede or occur during CNS O₂ toxicity.