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Vol. 282, Issue 3, 1181-1186, 1997
-Aminobutyric AcidA Receptors
Monash University, Department of Anesthesia, Monash Medical Centre,
Clayton, Victoria, Australia 3168
In this study, we investigated the interaction of propofol (a compound
used widely as an intravenous anesthetic) with 
-aminobutyric acidA (GABAA) and
delta opioid receptors at the level of the spinal cord.
Nociceptive thresholds were measured in rats through the use of
electrical current testing (ECT) and tail-flick latency. Full recovery
from sedation occurred 36.3 ± 1.7 min (mean ± S.E.M.; n = 20) after 40 mg/kg propofol i.p. Forty minutes
after administration, there was residual antinociception when assessed
by ECT but not when assessed by noxious heat. The ECT antinociceptive
effects of propofol at tail but not neck sites were suppressed by
intrathecal injection of the GABAA antagonists
bicuculline and SR-95531 and the delta opioid antagonist
naltrindole. These results suggest that there is an interaction between
propofol and antagonists at receptors in the caudal segments of the
spinal cord responsible for tail innervation. Antagonist dose-response
curves were compared with those for suppression of intrathecal
midazolam-induced antinociception. All intrathecal antagonists reversed
the antinociceptive effect of propofol with the same dose-response
curves as those previously obtained for suppression of the effect of
intrathecal midazolam. We conclude that propofol, when given
intraperitoneally, produces antinociception in rats through an
interaction with spinal GABAA receptors. This
combination leads to activation of a spinal cord system involving a
delta opioid receptor; the same mechanisms involved with
midazolam-induced spinal antinociception.
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