Opioid footshock-induced analgesia in mice acutely falls by stress prolongation

Physiol Behav. 1993 Jun;53(6):1115-9. doi: 10.1016/0031-9384(93)90367-o.

Abstract

The application of 80 footshocks (S-80) to mice induces a decrease in nociceptive responses as measured by the tail-flick test, which is opioid mediated as well as prevented by naloxone (10 mg/kg, SC). When the stress is prolonged up to 240 shocks (S-240) (i.e., from 6 min 40 s to 20 min), no analgesia can be seen immediately after the stress. We have examined the two most obvious possibilities, but they do not seem to be responsible for this fact. When morphine (1-5 mg/kg IP) is injected in the S-240 situation, a potentiation of its analgesic effects is seen, so that a desensitization of mu opioid receptors is unlikely. On the other hand, although cortisol (3-30 mg/kg IP) inhibits the analgesic response to S-80, metyrapone (40 and 80 mg/kg IP) and cortexolone (3-18 mg/kg IP) do not cause S-240 to be analgesic. Thus, an increase of endogenous glucocorticoids released during the long-duration stress does not seem responsible for the lack of analgesia after S-240.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Arousal / drug effects*
  • Arousal / physiology
  • Cortodoxone / pharmacology
  • Dose-Response Relationship, Drug
  • Electroshock
  • Hydrocortisone / pharmacology
  • Injections, Intraperitoneal
  • Injections, Subcutaneous
  • Male
  • Metyrapone / pharmacology
  • Mice
  • Morphine / pharmacology*
  • Naloxone / pharmacology*
  • Pain Threshold / drug effects*
  • Pain Threshold / physiology
  • Reaction Time / drug effects
  • Reaction Time / physiology
  • Receptors, Opioid / drug effects*
  • Receptors, Opioid / physiology

Substances

  • Receptors, Opioid
  • Naloxone
  • Morphine
  • Cortodoxone
  • Hydrocortisone
  • Metyrapone