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ANESTHETIC PHARMACOLOGY

Xenon Inhibits but N₂O Enhances Ketamine-Induced c-Fos Expression in the Rat Posterior Cingulate and Retrosplenial Cortices

Department of Anesthesiology, Kansai Medical University, Osaka, Japan

Address correspondence and reprint requests to Shin-ichi Nakao, Department of Anesthesiology, Kansai Medical University, Moriguchi, Osaka 570-8507, Japan. Address e-mail to nakaos{at}takii.kmu.ac.jp

Both nitrous oxide (N₂O) and xenon are N-methyl-D-aspartate receptor antagonists that have psychotomimetic effects and cause neuronal injuries in the posterior cingulate and retrosplenial cortices. We investigated the effect of xenon, xenon with ketamine, N₂O, and N₂O with ketamine on c-Fos expression in the rat posterior cingulate and retrosplenial cortices, a marker of psychotomimetic effects. Brain sections were prepared, and c-Fos expression was detected with immunohistochemical methods. A loss of microtubule-associated protein 2, a marker of neuronal injury, was also investigated. The number of Fos-like immunoreactivity positive cells by ketamine IV at a dose of 5 mg/kg under 70% N₂O (128 ± 12 cells per 0.5 mm²) was significantly more than those under 30% (15 ± 2 cells per 0.5 mm²) and 70% xenon (2 ± 1 cells per 0.5 mm²). Despite differences in c-fos immunoreactivity, there was no loss of microtubule-associated protein 2 immunoreactivity in any group examined. Xenon may suppress the adverse neuronal effects of ketamine, and combined use of xenon and ketamine seems to be safe in respect to neuronal adverse effects.

Implications: Xenon may suppress adverse neuronal effects of ketamine. Conversely, combined use of N₂O and ketamine may increase the risk of neuronal adverse effects, such as psychotomimetic effects.

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