Related Experiment Video

Updated: Apr 18, 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

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BTP2, a store-operated calcium channel inhibitor, attenuates morphine antinociceptive tolerance in rats

Weibo Xiao1, Feng Xiao2, Yingying Zhang3

  • 1Department of Anesthesiology, Loudi Central Hospital, Loudi, China.

Frontiers in Neuroscience
|April 17, 2026
PubMed
Abstract

Insights

BTP2, a store-operated calcium channel inhibitor, reduces morphine tolerance by suppressing spinal cord inflammation and astrocyte activation. This offers a potential new treatment for chronic pain management.

Area of Science:

  • Neuroscience
  • Pharmacology
  • Pain Management

Background:

  • Morphine antinociceptive tolerance is a significant clinical challenge.
  • Spinal cord glial cell activation and neuroinflammation are implicated in morphine tolerance.
  • BTP2, a store-operated calcium channel inhibitor, exhibits anti-inflammatory effects in the central nervous system.

Purpose of the Study:

  • To investigate BTP2's effect on morphine antinociceptive tolerance development.
  • To assess BTP2's impact on glial cell-derived pro-inflammatory cytokines.
  • To explore BTP2's potential in reversing established morphine tolerance.

Main Methods:

  • A rat model of morphine antinociceptive tolerance was established via intrathecal morphine.
  • BTP2 was administered intrathecally to either prevent or reverse morphine tolerance.
  • Immunohistochemistry and cytokine analysis were used to assess spinal cord changes.

Main Results:

  • BTP2 attenuated the development of morphine tolerance.
  • BTP2 partially reversed established morphine tolerance.
  • BTP2 suppressed chronic morphine-induced astrocyte activation, ERK activation, and pro-inflammatory cytokine production (TNF-α, Il-1β).

Conclusions:

  • BTP2 demonstrates potential as a therapeutic agent for morphine antinociceptive tolerance.
  • Store-operated calcium channels play a crucial role in morphine antinociceptive tolerance.
Keywords:
BTP2ERKGFAPmorphinestore-operated calcium channelstolerance

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