Human brain sodium channels as one of the molecular target sites for the new intravenous anaesthetic propofol (2,6-diisopropylphenol).
Single sodium channels from human brain cortex tissue were incorporated into voltage-clamped planar lipid bilayers in the presence of batrachotoxin and studied with various doses of the new anaesthetic compound propofol (2,6-diisopropylphenol). Propofol was found to depress two major sodium channel functions, leading to a reduction of the time-averaged fractional channel open-time (half-maximal blocking concentration, ED50, 20 microM; maximal block 28%) and an interaction with the steady-state activation. These effects occurred at clinically relevant serum concentrations, suggesting the human brain sodium channel as one of the molecular target sites of action for propofol.
Frenkel
C
C
Department of Anesthesiology, Cornell University Medical College, New York, N.Y. 10021.
Urban
B W
BW
D001665:Binding Sites; D001923:Brain Chemistry; D004553:Electric Conductivity; D006801:Humans; D008051:Lipid Bilayers / Q000737:chemistry; D008564:Membrane Potentials / Q000187:drug effects; D015742:Propofol / Q000494:pharmacology*; D015222:Sodium Channels / Q000187:drug effects*
D008051:Lipid Bilayers; D015222:Sodium Channels; D015742:Propofol