Hyperbaric oxygen depolarizes solitary complex neurons in tissue slices of rat medulla oblongata.
Hyperbaric oxygen depolarizes solitary complex neurons in tissue slices of rat medulla oblongata.
复制标题
高压氧使大鼠延髓组织切片中的孤立复杂神经元去极化。
DOI:
10.1007/0-306-46825-5_45
复制
发表时间:
2000
影响因子:
--
通讯作者:
Dean,JB
中科院分区:
文献类型:
--
作者:
Mulkey,DK;Henderson3rd,RA;Dean,JB
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 O2on the membrane potential and firing rate of neurons in the mammalian brainstem. Likewise, no study has ever determined the effects of ≤3 ATA pressureper seon 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 pressureper 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 (Rm)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, pO223–34 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, Rmeither increased (n 5). decreased (n 2) or was unchanged (n=⌋). Three of 8 neurons depolarized by HBOP2were also depolarized by hyperbaric helium, usually with an additional change in RmWe conclude that hydrostatic (helium) pressure and HBO2independently 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 O2toxicity.