IMPLICATIONS: We have demonstrated that propofol depressed epileptiform activity in rat hippocampal slices. Adenosine neuromodulation through the A 1 receptor may contribute to the anticonvulsant action of propofol.

Propofol is an IV anesthetic that may have both pro-and anticonvulsant actions in vivo. An increase in the mean spike number and an extension of spike distribution in the electrocorticogram after propofol administration were observed in patients with seizure disorders (1, 2). In contrast, propofol was used successfully in the treatment of status epilepticus (3) and has been reported to decrease the duration of seizure activity during electroconvulsive therapy (4). Numerous animal studies have shown that propofol possesses anticonvulsant properties against seizures induced by electroshock (5), bupivacaine (6), and some chemoconvulsants (7). An anticonvulsant action of propofol is supported by electrophysiological studies, which have demonstrated that propofol enhances inhibitory γ-aminobutyric acid (GABA) A receptor-mediated responses and directly activates GABA A receptors (8, 9). There is clinical (10) and experimental (11) evidence that adenosinergic neurotransmission can modulate certain types of seizures. Anticonvulsant effects have been reported after activation of the adenosine system with an adenosine A 1 receptor agonist (12). However, an electrophysiological study of the interaction of propofol with the adenosine system has not been reported. In the present study, we investigated the contribution of adenosine neuromodulation to propofol-induced depression of excitatory synaptic transmission.

Methods

All of the experimental procedures used in this study were reviewed and approved by the animal care and use committee of our institute.