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.

journal_name

Behav Brain Res

authors

Johnston IN,Westbrook RF

doi

10.1016/j.bbr.2003.08.022

subject

Has Abstract

pub_date

2004-05-05 00:00:00

pages

151-8

issue

1-2

eissn

0166-4328

issn

1872-7549

pii

S0166432803003516

journal_volume

151

pub_type

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