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Vol. 290, Issue 1, 362-367, July 1999
Department of Anesthesia, Stanford University School of Medicine,
Stanford, California
Ethanol is a general anesthetic agent as defined by abolition of
movement in response to noxious stimulation. This anesthetic endpoint
is due to spinal anesthetic actions. This study was designed to test
the hypothesis that ethanol acts directly on motor neurons to inhibit
excitatory synaptic transmission at glutamate receptors. Whole cell
recordings were made in visually identified motor neurons in spinal
cord slices from 14- to 23-day-old rats. Currents were evoked by
stimulating a dorsal root fragment or by brief pulses of glutamate.
Ethanol at general anesthetic concentrations (50-200 mM) depressed
both responses. Ethanol also depressed glutamate-evoked responses in
the presence of tetrodotoxin (300 nM), showing that its actions are
postsynaptic. Block of inhibitory 
-aminobutyric acidA
and glycine receptors by bicuculline (50 µM) and strychnine (5 µM), respectively, did not significantly reduce the effects of
ethanol on glutamate currents. Ethanol also depressed glutamate-evoked currents when the inhibitory receptors were blocked and either D,L-2-amino-5-phosphonopentanoic acid (40 µM)
or 6-cyano-7-nitroquinoxaline-2,3-dione disodium (10 µM) were applied
to block N-methyl-D-aspartate or 
-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid/kainate
receptors, respectively. The results show that ethanol exerts direct
depressant effects on both
-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid and
N-methyl-D-aspartate glutamate currents in
motor neurons. Enhancement of -aminobutyric acidA and
glycine inhibition is not required for this effect. Direct depression
of glutamatergic excitatory transmission by a postsynaptic action on
motor neurons thus may contribute to general anesthesia as defined by
immobility in response to a noxious stimulus.
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