Ethanol, usually studied in relation to intoxication, is also capable
of producing general anesthesia. The most common standard of anestheti
c potency is the concentration which produces immobility in response t
o a noxious stimulus. This concentration will be referred to as the an
esthetic concentration. Immobilization is a spinal effect. Ethanol eff
ects were studied in spinal cord from 2-7-day-old rats at concentratio
ns which included the anesthetic concentration in both adult rats (97
mM) and 6-7-day-old rats (235 mM). At neonatal but not adult anestheti
c concentrations, ethanol depressed monosynaptic reflex amplitude (med
iated by glutamate AMPA receptors + compound action potential). At bot
h neonatal and adult anesthetic concentrations ethanol reversibly depr
essed the population excitatory postsynaptic potential (pEPSP) (glutam
ate AMPA and NMDA receptors), the slow ventral root potential (NMDA metabotropic receptors), and the dorsal root potential (GABA(A) recept
ors, via glutamate-excited interneurons). Effects were greater on NMDA
receptor-mediated components than on AMPA-receptor-mediated component
s of the pEPSP and greater on NMDA than on metabotropic receptor-media
ted components of the slow ventral root potential. The profile of etha
nol effects on spinal cord resembles that of inhalation general anesth
etics. The results show that both AMPA and NMDA receptor-mediated tran
smission are sensitive to ethanol and that enhancement of GABAergic ne
urotransmission is overridden by depression of excitation to the inter
neurons. They provide no obvious explanation far ethanol's lower gener
al anesthetic potency in the neonate. (C) 1997 Elsevier Science B.V.