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Updated: Jul 3, 2026

Assessment of Morphine-induced Hyperalgesia and Analgesic Tolerance in Mice Using Thermal and Mechanical Nociceptive Modalities
Published on: July 29, 2014
Prolonged morphine application modulates Bax and Hsp70 levels in primary rat neurons
Qiuyue Chen1, Jia Cui, Yan Zhang
1Laboratory of Neurobiology and State Key Laboratory of Biomembrane and Membrane Biotechnology, College of Life Sciences, Peking University, Beijing 100871, China.
Morphine protects rat neurons from cell death by reducing levels of pro-apoptotic protein Bax and molecular chaperone Hsp70. This suggests a potential neuroprotective role for morphine in certain conditions.
Area of Science:
- Neuroscience
- Pharmacology
- Cell Biology
Background:
- Morphine, a long-used pain reliever, has conflicting data regarding its effects on neuronal survival.
- Some studies indicate morphine may induce neuronal apoptosis, while others suggest neuroprotective properties.
Purpose of the Study:
- To investigate the impact of morphine on neuronal cell death.
- To determine the effect of morphine on the expression of the pro-apoptotic protein Bax and the molecular chaperone Hsp70.
Main Methods:
- Primary rat neurons were cultured and treated with varying concentrations of morphine.
- Cell death was induced using serum deprivation and staurosporine.
- Levels of Bax and Hsp70 were measured following morphine treatment.
Main Results:
- Prolonged administration of 1µM morphine for 5 days protected primary rat neurons against serum deprivation-induced cell death.
- Morphine treatment led to decreased levels of both Bax and Hsp70 in cultured neurons.
Conclusions:
- Morphine exhibits a protective role against neuronal cell death induced by serum deprivation and staurosporine.
- The observed neuroprotection is associated with reduced expression of Bax and Hsp70.
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