To investigate propofol's effects on ionic currents induced by γ-aminobutyric acid (GABA) and glycine as well as on those produced by the nicotinic acetylcholine- and glutamate-responsive channels, rat dorsal raphe neurons were acutely dissociated and the nystatin-perforated patch-clamp technique under voltage- clamp conditions was used to observe their responses to the administration of propofol. Propofol evoked ion currents in a dose-dependent manner, and propofol (10⁣4 M) was used to elicit ion currents through the activation of GABAA, glycine, nicotinic acetylcholine and glutamate receptors. Propofol at a clinically relevant concentration (10⁣5 M) potentiated GABAA-, glycine- and NMDA receptor-mediated currents. The potentiating action of propofol on GABAA-, glycine- and NMDA receptor-mediated responses involved neither opioid receptors nor G-proteins. Apparently, propofol modulates inhibitory and excitatory neurotransmitter-activated ion channels either by acting directly on the receptors or by potentiating the effects of the neurotransmitters, and this modulation appears to be responsible for the majority of the anaesthetic and/or adverse effects.