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Acute and conditioned sickness reduces morphine analgesia
Ian N Johnston1, R Frederick Westbrook
1Department of Psychology, University of Colorado, Boulder, CO 80303-0345, USA. johnstoi@psych.colorado.edu
Behavioural Brain Research
|June 12, 2003
Summary
Illness-inducing agents like lithium chloride (LiCl) and lipopolysaccharides (LPS) can reduce morphine analgesia. This effect occurs through endogenous antianalgesic mechanisms, not just increased pain sensitivity.
Area of Science:
- Neuroscience
- Pharmacology
- Pain Research
Background:
- Illness can induce hyperalgesia (increased pain sensitivity) via toxins like lithium chloride (LiCl) or lipopolysaccharides (LPS).
- The neurocircuitry involved in illness-induced hyperalgesia shares similarities with mechanisms underlying morphine analgesic tolerance.
Purpose of the Study:
- To investigate if illness-inducing agents (LiCl, LPS) or associated cues reduce morphine analgesia.
- To determine if illness-induced tolerance is mediated by increased pain sensitivity or other mechanisms.
Main Methods:
- Rats were injected with LiCl or LPS, or exposed to LiCl-associated cues.
- Morphine analgesia was assessed using the tail flick and hot plate tests.
- Pain sensitivity and contextual learning were evaluated.
Main Results:
- LiCl and LPS injections reduced morphine analgesia at 24 hours, with LiCl also showing effects at 40 minutes.
- Contextual cues associated with LiCl also decreased morphine analgesia.
- These reductions in analgesia occurred without significant hyperalgesia, suggesting tolerance is not solely due to increased pain.
Conclusions:
- Illness-inducing agents activate endogenous antianalgesic mechanisms.
- These mechanisms antagonize morphine analgesia independently of increased pain sensitivity.
- Environmental cues associated with illness can also impair opioid analgesia.