Department of Organismal Biology and Anatomy, Chicago, IL, USA.
J Appl Physiol (1985). 2010 Sep;109(3):820-9. doi: 10.1152/japplphysiol.91430.2008. Epub 2010 Jun 17.
The first study, described in the companion article, reports that acute exposure of rat hippocampal slices to either hyperbaric oxygen (HBO: 2.84 and 4.54 atmospheres absolute, ATA) or normobaric reoxygenation (NBOreox; i.e., normobaric hyperoxia: 0.6 or 0.0→0.95 ATA) stimulates synchronous orthodromic activity in CA1 neurons, which includes activation of O2-induced potentiation (OxIP) and, in some cases, hyperexcitability (secondary population spikes, sPS). In this second study we tested the hypothesis that HBO and NBOreox increase orthodromic activity of CA1 neurons (oPS, orthodromic population spike) and OxIP via a combination of both increased excitatory synaptic transmission (field excitatory postsynaptic potential, fEPSP) and intrinsic excitability (antidromic population spike, aPS). HBO and NBOreox increased the oPS but rarely increased or potentiated the fEPSP. HBO exposure produced epileptiform antidromic activity, which was abolished during inhibition of fast GABAergic and glutamatergic synaptic transmission. Decreasing O2 from 0.95 ATA (control) to 0.6 ATA (intermediate O2) or 0.0 ATA (hypoxia) reversibly abolished the fEPSP, and reoxygenation rarely induced potentiation of the fEPSP or aPS. Intracellular recordings and antidromic field potential recordings, however, revealed that synaptic transmission and neuronal excitability were preserved, albeit at lower levels, in 0.60 ATA O2. Together, these data indicate that 1) the changes in excitatory postsynaptic activity are not required for stimulation of the oPS during and HBO/NBOreox or for activation of OxIP, suggesting the latter is a form of intrinsic plasticity; 2) HBO disinhibits spontaneous synaptic transmission to induce epileptiform activity; and 3) although synchronous synaptic activation of the CA1 neuronal population requires hyperoxia (i.e., 0.95 ATA O2), synaptic activation of individual CA1 neurons does not.
第一篇研究论文（见随附文章）报道，急性暴露于高压氧（HBO：2.84 和 4.54 个大气压绝对，ATA）或常压复氧（NBOreox；即常压高氧：0.6 或 0.0→0.95 ATA）会刺激 CA1 神经元的同步传入活动，包括 O2 诱导的增强（OxIP）的激活，并且在某些情况下，兴奋性过度（继发性群体峰，sPS）。在第二项研究中，我们检验了 HBO 和 NBOreox 通过增加兴奋性突触传递（场兴奋性突触后电位，fEPSP）和内在兴奋性（逆行群体峰，aPS）的组合来增加 CA1 神经元的传入活动（oPS，传入群体峰）和 OxIP 的假说。HBO 和 NBOreox 增加了 oPS，但很少增加或增强 fEPSP。HBO 暴露产生了癫痫样逆行活动，在快速 GABA 能和谷氨酸能突触传递抑制期间被消除。将 O2 从 0.95 ATA（对照）降低到 0.6 ATA（中间 O2）或 0.0 ATA（缺氧）可使 fEPSP 可逆性消失，而复氧很少引起 fEPSP 或 aPS 的增强。然而，细胞内记录和逆行场电位记录显示，在 0.60 ATA O2 中，突触传递和神经元兴奋性虽然保持不变，但水平较低。总的来说，这些数据表明：1）兴奋性突触后活动的变化对于刺激 HBO/NBOreox 期间的 oPS 和 OxIP 的激活不是必需的，这表明后者是一种内在可塑性；2）HBO 去抑制自发突触传递以诱导癫痫样活动；3）尽管 CA1 神经元群体的同步突触激活需要高氧（即 0.95 ATA O2），但单个 CA1 神经元的突触激活不需要。
