Korean J Physiol Pharmacol.  2001 Apr;5(2):189-197.

Effect of propofol on ion channels in acutely dissociated dorsal raphe neuron of Sprague-Dawley rats

• Lee BJ
• Kwon MI
• Shin MC
• Kim YJ
• Kim CJ
• Kim SA
• Kim EH
• Chung JH

Abstract

To investigate propofol's effects on ionic currents induced by gamma-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.

Keyword

Propofol; GABA; Glycine; Glutamic acid; Patch-clamp technic

MeSH Terms

Acetylcholine
Animals
gamma-Aminobutyric Acid
Glutamic Acid
Glycine
GTP-Binding Proteins
Ion Channels*
N-Methylaspartate
Neurons*
Neurotransmitter Agents
Patch-Clamp Techniques
Propofol*
Rats
Rats, Sprague-Dawley*
Receptors, Glutamate
Receptors, Opioid
Acetylcholine
GTP-Binding Proteins
Glutamic Acid
Glycine
Ion Channels
N-Methylaspartate
Neurotransmitter Agents
Propofol
Receptors, Glutamate
Receptors, Opioid
gamma-Aminobutyric Acid