Steady-state pattern visual evoked potentials were recorded from the surface of the cat primary visual cortex before and after the intravenous administration of physostigmine, an agent that blocks the enzyme responsible for the breakdown of synaptically released acetylcholine. Under pentobarbital anesthesia, physostigmine increased the amplitude and changed the phase of the second response harmonic of the visual evoked potential, whereas the amplitude and phase of the fourth harmonic were not affected. These effects persisted for 15 to 45 minutes and were blocked by prior treatment with scopolamine or atropine. In addition, scopolamine or atropine administered 5 to 10 minutes after physostigmine returned the visual evoked potential to the baseline state. In comparison, when nitrous oxide was used, physostigmine caused a marked reduction in visual evoked potential amplitude, an effect that was reversed by subsequent atropine. These results indicate that the cholinergic system influences the visual evoked potential via a muscarinic pathway and that this influence is strongly affected by the anesthetic regimen used.
- Visual cortex
- Visual evoked potential (VEP)
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