Effects of intrathecal 6-hydroxydopamine, α1 and α2 adrenergic receptor antagonists on antinociception of propofol in mice
Article first published online: 27 JAN 2005
DOI: 10.1111/j.1745-7254.2005.00033.x
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How to Cite
GE, Z.-j., ZENG, Y.-m. and TAN, Y.-f. (2005), Effects of intrathecal 6-hydroxydopamine, α1 and α2 adrenergic receptor antagonists on antinociception of propofol in mice. Acta Pharmacologica Sinica, 26: 186–191. doi: 10.1111/j.1745-7254.2005.00033.x
Publication History
- Issue published online: 27 JAN 2005
- Article first published online: 27 JAN 2005
- Received 2004-07-21; Accepted 2004-10-19
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Keywords:
- propofol;
- spinal cord;
- antinociception;
- prazosin;
- yohimbine;
- norepinephrine
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 tail-immersion 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 tail-immersion 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.

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