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Endogenous dynorphin modulates calcium-mediated antinociception in mice
1Department of Pharmacology and Toxicology, Virginia Commonwealth University/Medical College of Virginia, Richmond 23298-0613.
Pharmacology, Biochemistry, and Behavior
|June 1, 1993
Summary
Calcium administration can reduce pain by releasing Met-enkephalin, but its effectiveness varies. This study found that during diminished pain relief, calcium also releases dynorphin, which can block pain reduction.
Area of Science:
- Neuroscience
- Pharmacology
- Pain Research
Background:
- Previous research indicated that intrathecal (IT) calcium administration induces antinociception via spinal Met-enkephalin release.
- However, the antinociceptive effects of calcium are not always consistent in the tail-flick test.
Purpose of the Study:
- To investigate the mechanism behind the variable antinociceptive effects of calcium.
- To determine the role of endogenous dynorphin release in modulating calcium-induced antinociception.
Main Methods:
- Mice received intrathecal (IT) calcium injections.
- Pretreatment with vehicle, pentobarbital, naloxone, or norbinaltorphimine (BNI) was administered.
- The effects of various dynorphin fragments (Dyn 1-17, Dyn 1-13, Dyn 1-8) and antiserum to Dyn (1-13) on antinociception were assessed.
Main Results:
- Calcium administration alone showed poor antinociception in some cases.
- Pentobarbital, naloxone, and BNI pretreatment restored calcium's antinociceptive effects.
- Specific dynorphin fragments (Dyn 1-17, Dyn 1-13) blocked restored antinociception, while antiserum to Dyn (1-13) restored it.
Conclusions:
- Calcium administration stimulates endogenous dynorphin release, which can inhibit antinociception.
- The effectiveness of calcium-mediated antinociception is modulated by the balance between Met-enkephalin and dynorphin.
- Targeting dynorphin pathways may enhance calcium's pain-relieving potential.