Inhibition of morphine analgesia by lithium: role of peripheral and central opioid receptors.

Abstract

Intraperitoneal (i.p.) administration of lithium chloride (LiCl) has two effects on pain sensation: (1) it induces a transient hyperalgesia that is reversed by intracerebroventricular (i.c.v.) or intrathecal (i.t.) administration of the opioid receptor antagonist naloxone or by peripheral administration of the quaternary compound naloxone methiodide [Behav. Neurosci. 114 (2000) 1183]; (2) it produces a long-lasting (24 h) reduction in morphine analgesia and does so in the absence of hyperalgesia [Behav. Brain Res. 142 (2003) 89]. We confirmed that rats administered with LiCl showed a reduction in analgesia when administered morphine 24 h later. We also found that morphine analgesia was restored if LiCl had been preceded by i.p. or i.c.v. administration of naloxone or by i.p. administration of naloxone methiodide. However, i.p. administration of naloxone methiodide prior to testing 24 h after an injection with LiCl did not restore morphine analgesia. Thus, activity at peripheral and central opioid receptors is necessary for the inhibition of morphine analgesia by LiCl, but peripheral opioid receptors are not critical for the expression of this inhibition.

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@article{Johnston2004InhibitionOM, title={Inhibition of morphine analgesia by lithium: role of peripheral and central opioid receptors.}, author={Ian N. Johnston and Reginald Frederick Westbrook}, journal={Behavioural brain research}, year={2004}, volume={151 1-2}, pages={151-8} }