Effects of intrathecal 6-hydroxydopamine, α1 and α2 adrenergic receptor antagonists on antinociception of propofol in mice
Abstract
Aim: To investigate the relationship between spinal cord norepinephrine, α1 and
α2 adrenergic receptors and antinociception of propofol in mice. Methods:
Kunming mice were used. Antinociceptive tests were investigated with the tailimmersion
test and the acetic acid-induced writhing test. The effects of subcutaneous
(sc), intrathecal (ith) and intracerebroventricular (icv) injection propofol
on pain threshold were observed. The influences of pretreatment with ith 6-
hydroxydopamine, α1R antagonist prazosin, or α2R antagonist yohimbine on the
antinociception of propofol were studied. Results: Significant antinociception
was produced by propofol (25, 50 mg/kg, sc) and propofol (20, 40 μg, ith) in tailimmersion
test and acetic the acid-induced writhing test (P<0.05 or P<0.01). Icv
propofol (10, 20, and 40 μg) did not produce any effect on pain threshold in mice
(P>0.05). The 6-hydroxydopamine (5 and 10 μg), prazosin (5 and 10 μg), or
yohimbine (5 and 10 μg) ith alone did not affect basal tai-flick latency (TFL) in
conscious mice, but significantly reduced the TFL as measured by tail-immersion
test in propofol (50 mg/kg, sc)-treated mice, compared with basal TFL and vehicle
groups (P<0.05 or P<0.01). Conclusion: The spinal cord is a target of
propofol antinociception. In mice propofol antinociception is partly mediated by
spinal norepinephrine, α1R and α2R.
Keywords:
α2 adrenergic receptors and antinociception of propofol in mice. Methods:
Kunming mice were used. Antinociceptive tests were investigated with the tailimmersion
test and the acetic acid-induced writhing test. The effects of subcutaneous
(sc), intrathecal (ith) and intracerebroventricular (icv) injection propofol
on pain threshold were observed. The influences of pretreatment with ith 6-
hydroxydopamine, α1R antagonist prazosin, or α2R antagonist yohimbine on the
antinociception of propofol were studied. Results: Significant antinociception
was produced by propofol (25, 50 mg/kg, sc) and propofol (20, 40 μg, ith) in tailimmersion
test and acetic the acid-induced writhing test (P<0.05 or P<0.01). Icv
propofol (10, 20, and 40 μg) did not produce any effect on pain threshold in mice
(P>0.05). The 6-hydroxydopamine (5 and 10 μg), prazosin (5 and 10 μg), or
yohimbine (5 and 10 μg) ith alone did not affect basal tai-flick latency (TFL) in
conscious mice, but significantly reduced the TFL as measured by tail-immersion
test in propofol (50 mg/kg, sc)-treated mice, compared with basal TFL and vehicle
groups (P<0.05 or P<0.01). Conclusion: The spinal cord is a target of
propofol antinociception. In mice propofol antinociception is partly mediated by
spinal norepinephrine, α1R and α2R.