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Updated: Jul 4, 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

Continuous treatment with morphine increases diazepam binding inhibitor mRNA in mouse brain

M Katsura1, A Hara, A Higo

  • 1Department of Pharmacology, Kawasaki Medical School, Matsushima, Kurashiki, Japan.

Journal of Neurochemistry
|December 1, 1998
PubMed

Insights

Chronic morphine use increases diazepam binding inhibitor (DBI) mRNA brain expression, especially during withdrawal. Naloxone blocks this effect, indicating opioid receptor involvement in DBI mRNA regulation.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Pharmacology

Background:

  • Diazepam binding inhibitor (DBI) is involved in the regulation of GABAergic neurotransmission.
  • Opioid receptors play a crucial role in pain modulation and addiction.
  • Understanding the molecular mechanisms underlying opioid dependence is essential for developing effective treatments.

Purpose of the Study:

  • To investigate the effects of acute and chronic morphine administration on DBI mRNA expression in the mouse brain.
  • To determine the role of opioid receptors in mediating changes in DBI mRNA levels during morphine treatment and withdrawal.

Main Methods:

  • Mice were treated with acute or chronic morphine.
  • Morphine dependence and withdrawal were induced.
  • Cerebral DBI mRNA expression was quantified using molecular techniques.
  • The effect of naloxone on DBI mRNA expression was examined.

Main Results:

  • Acute morphine administration did not alter DBI mRNA expression.
  • Chronic morphine treatment led to a significant increase in cerebral DBI mRNA expression.
  • This increase was more pronounced in morphine-withdrawn mice.
  • Co-administration of naloxone with morphine prevented the increase in DBI mRNA expression.

Conclusions:

  • Chronic morphine exposure, acting through opioid receptors, upregulates DBI mRNA expression in the brain.
  • DBI mRNA levels are sensitive to opioid withdrawal, suggesting a role in the withdrawal syndrome.
  • These findings highlight a potential molecular pathway linking opioid receptor activation to changes in DBI expression.

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