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Updated: Oct 7, 2026

Assessment of Morphine-induced Hyperalgesia and Analgesic Tolerance in Mice Using Thermal and Mechanical Nociceptive Modalities
07:23

Assessment of Morphine-induced Hyperalgesia and Analgesic Tolerance in Mice Using Thermal and Mechanical Nociceptive Modalities

Published on: July 29, 2014

Loss of locomotor sensitisation in response to morphine in D1 receptor deficient mice

A Becker1, G Grecksch, J Kraus

  • 1Otto-von-Guericke Universität, Medizinische Fakultät, Institut für Pharmakologie und Toxikologie, Magdeburg, Germany. axel.becker@medizin.uni-magdeburg.de

Naunyn-Schmiedeberg'S Archives of Pharmacology
|June 1, 2001
PubMed

Insights

Mice without D1 receptors showed increased pain relief from morphine but lacked the typical increase in movement after repeated doses. This suggests D1 receptors are key to morphine

Area of Science:

  • Neuroscience
  • Pharmacology
  • Molecular Biology

Background:

  • Dopamine D1 receptors play a crucial role in modulating various physiological processes.
  • The specific involvement of D1 receptors in morphine's effects, including analgesia and behavioral sensitization, remains incompletely understood.
  • Understanding these mechanisms is vital for developing safer and more effective pain management strategies.

Purpose of the Study:

  • To investigate the role of D1 receptors in morphine-induced antinociception (pain relief) and locomotor sensitization.
  • To determine how the absence of D1 receptors affects the development of tolerance and behavioral changes following chronic morphine administration.
  • To explore the neurobiological underpinnings, specifically mu-opioid receptor levels, associated with altered morphine responses in D1 receptor-deficient mice.

Main Methods:

  • Utilized D1 receptor-deficient (knockout) and wild-type (control) mice.
  • Assessed antinociception using the hot-plate test following acute morphine administration.
  • Evaluated locomotor activity and sensitization after chronic morphine treatment.
  • Quantified levels of immunoreactive mu-opioid receptors in specific brain regions (dorsal striatum, spinal cord) using immunohistochemistry.

Main Results:

  • D1 receptor-deficient mice exhibited enhanced antinociception compared to wild-type mice after acute morphine injection.
  • Chronic morphine administration led to locomotor sensitization in wild-type mice but not in D1 receptor-deficient mice.
  • D1 receptor deficiency was associated with reduced mu-opioid receptor levels in the dorsal striatum, but not in the spinal cord.

Conclusions:

  • D1 receptors significantly modulate morphine-induced antinociception and locomotor activity.
  • The absence of D1 receptors impairs the development of morphine-induced locomotor sensitization, potentially linked to altered mu-opioid receptor expression in the striatum.
  • These findings highlight the critical role of D1 receptors in the complex neuroadaptations underlying opioid responses.

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