Abstract
The adult pseudoflash, produced by readmitting O2 following an hypoxic period, can be affected by neural activity. Electrical stimulation restores declining pseudo-flashes and increases the rate of hypoxic glow rise. Perfusion with eserine enhances the ability to produce pseudoflashes. Transection of nerves destroys the pseudoflash response. Nerve impulses were not observed during the pseudoflash. A possibility suggested is that previous neural activity may serve as a priming mechanism.

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