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. 2010 Jun 17;109(3):820–829. doi: 10.1152/japplphysiol.91430.2008

Fig. 10.

Fig. 10.

Working model derived from our two studies (Ref. 9 and present study) that postulates how acute exposure to HBO may stimulate CA1 neurons causing increased excitability and OxIP. This model may also be applied to the phenomenon of OxIP of the oPS caused by NBOreox from 0.60 to 0.95 ATA O2. A: in 0.95 ATA O2 (control conditions), excitability of CA1 pyramidal neurons (open and shaded bars) is regulated by active synaptic input from GABAergic interneurons [open box, inhibitory (−) neurons] and from Schaffer-commissural collaterals and intrinsic membrane properties of the pyramidal neurons themselves. Moreover, with submaximal stimulation of the Schaffer-commissural collaterals, as used in our studies, only a fraction of neurons are activated (open), whereas others are silent (shaded). B: during HBO, our study shows that the oPS is stimulated (1), and thus more CA1 pyramidal neurons are activated with Schaffer-commissural collateral stimulation. The elevated excitability of CA1 neurons during HBO is not dependent on a significant increase in the excitatory synapses of the Schaffer-commissural collaterals as measured by the lack of significant change on average of the fEPSP (2) or lack of change in axonal conduction as measured by the primary aPS (3). Finding that onset of antidromic sPS (3) during and following HBO exposure could be blocked by chemical synaptic blockade and mimicked by the application of picrotoxin (Ptx), which inhibits GABAergic ionotropic receptors, suggests that epileptiform activity occurs through GABAergic interneurons (shaded box) (4). The lack of effect of HBO on the primary aPS and fEPSP suggests that elevated excitability of CA1 pyramidal neurons results from a change in conduction from synapse to soma (5). Although it has yet to be determined, potential targets of O2 (and presumably ROS/RNS) that would increase orthodromic activation and induction of OxIP of the oPS include voltage-gated channels that regulate dendritic conduction and the threshold for action potential generation and gap junctions (shaded area).