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MODIFICATION OF ENDORPHIN/ENKEPHALIN ANALGESIA AND STRESS‐INDUCED ANALGESIA BY DIVALENT CATIONS, A CATION CHELATOR AND AN IONOPHORE

1 The possibility that divalent cations may antagonize opiate peptide analgesia and stress‐induced analgesia was examined. 2 Intracerebroventricular injection of low doses of Ca2+, Mn2+ and Mg2+ antagonized β‐endorphin and methionine‐enkephalin analgesia. Ba2+ and Cd2+ were without effect. 3 The ion...

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Published in:British journal of pharmacology 1982-02, Vol.75 (2), p.389-396
Main Authors: CHAPMAN, D.B., WAY, E. LEONG
Format: Article
Language:English
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Summary:1 The possibility that divalent cations may antagonize opiate peptide analgesia and stress‐induced analgesia was examined. 2 Intracerebroventricular injection of low doses of Ca2+, Mn2+ and Mg2+ antagonized β‐endorphin and methionine‐enkephalin analgesia. Ba2+ and Cd2+ were without effect. 3 The ionophore, A23187, significantly antagonized β‐endorphin analgesia and the effect was increased when a low dose of Ca2+ was injected at the same time as the ionophore. 4 Ethylene glycol tetraacetic acid (but not ethylenediamine tetraacetic acid) significantly potentiated endorphin analgesia. 5 Stress‐induced analgesia, as determined by increased tail‐flick latencies following intraperitoneal injection of acetic acid, was effectively antagonized by naloxone, Ca2+ and Mn2+. The frequency of writhing following acetic acid injection was increased by both naloxone and divalent metal ions, again suggesting antagonism of endogenous opiates. 6 These results confirm previous findings indicating that divalent metal ions (and especially Ca2+) may be involved in the actions of opiates.
ISSN:0007-1188
1476-5381
DOI:10.1111/j.1476-5381.1982.tb08799.x