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Updated: Sep 26, 2026

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

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L-type Ca(2+) channel blockers inhibit the development but not the expression of sensitization to morphine in mice

Qi Zhang1, Jun-Xu Li, Ji-Wang Zheng

  • 1Department of Neuropharmacology, National Institute on Drug Dependence, Peking University, 38 Xueyuan Road, Beijing 100083, PR China.

European Journal of Pharmacology
|April 23, 2003
PubMed

Insights

L-type Ca(2+) channel blockers reduce morphine-induced activity and inhibit the development of morphine sensitization. These blockers do not affect the expression of morphine sensitization, suggesting a role in addiction-related behaviors.

Area of Science:

  • Neuroscience
  • Pharmacology
  • Addiction Research

Background:

  • Opioid actions and L-type Ca(2+) channel blockers are linked.
  • Morphine sensitization is a model for drug addiction behaviors.
  • The effect of L-type Ca(2+) channel blockers on morphine sensitization is unknown.

Purpose of the Study:

  • To investigate the effects of nimodipine, nifedipine, and verapamil on morphine-induced locomotor activity.
  • To determine the impact of these blockers on the development and expression of morphine sensitization.

Main Methods:

  • Systematic study of three L-type Ca(2+) channel blockers.
  • Assessment of morphine-induced locomotor activity.
  • Evaluation of sensitization development and expression.

Main Results:

  • Nimodipine and verapamil attenuated morphine-induced locomotor activity; nifedipine showed a tendency to decrease it.
  • All three blockers inhibited the development of morphine sensitization.
  • No significant effect was observed on the expression of morphine sensitization.

Conclusions:

  • L-type Ca(2+) channel blockade attenuates morphine's locomotor effects.
  • Blocking L-type Ca(2+) channels inhibits the development, but not the expression, of morphine sensitization.
  • This suggests a potential role in modulating addiction-related processes.

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