PROPOFOL INHIBITS KETAMINE-INDUCED C-FOS EXPRESSION IN THE RAT POSTERIOR CINGULATE CORTEX

Ketamine, a noncompetitive N-methyl-D-aspartate (NMDA) receptor antago nist, has psychotomimetic activity. NMDA receptor antagonists cause mo rphological damage in the posterior cingulate cortex, which may be the brain region responsible for their psychotomimetic effects. Benzodiaz epines are effective in preventing these effects through gamma-aminobu tyric acid A (GABAA) receptor activation. We investigated the effect o f propofol, which has both GABAA receptor-activating and NMDA receptor -suppressing activity, on ketamine-induced c-fos expression in the rat posterior cingulate cortex. Propofol or vehicle was continuously infu sed IV. Fifteen minutes later, 100 mg/kg ketamine or isotonic sodium c hloride solution was injected intraperitoneally. Two hours later, brai n sections were prepared, and c-fos expression was detected using immu nohistochemical methods. Propofol significantly inhibited ketamine-ind uced c-fos expression in the posterior cingulate cortex. Propofol itse lf did not induce c-fos expression in this brain region. We conclude t hat propofol may be able to inhibit ketamine-induced psychotomimetic a ctivity and neuronal damage. Implications: In the present study, we de monstrated that the clinically relevant dose of propofol significantly inhibited ketamine-induced c-fos expression in the rat posterior cing ulate cortex. This finding implies that propofol may inhibit ketamine- induced psychotomimetic activity and neuronal damage.