Enhanced analgesic potency and reduced tolerance of morphine in 129/SvEv mice: evidence for a deficiency in GM1 ganglioside-regulated excitatory opioid receptor functions.

Abstract:

:10-fold higher doses in SW mice. Furthermore, cotreatment of 129/SvEv mice with morphine plus a low dose of naltrexone (ca. 0.1 microgram/kg) that markedly enhances and prolongs morphine's antinociceptive effects in SW mice did not enhance, and often attenuated6 h. The marked GM1-induced attenuation of morphine's antinociceptive effects in 129/SvEv mice may be due to conversion of some of the opioid receptors in these mice from an inhibitory Gi/Go-coupled to an excitatory Gs-coupled mode. Exogenous GM1 supplementation can, therefore, reverse the anomalous lack of morphine tolerance displayed by this mouse strain in comparison to SW and other mice. The present study may provide insights into factors that regulate the marked variability in nociceptive sensitivity and opioid tolerance/dependence liability among individual humans.

journal_name

Brain Res

journal_title

Brain research

authors

Crain SM,Shen K

doi

10.1016/s0006-8993(99)02446-4

subject

Has Abstract

pub_date

2000-02-21 00:00:00

pages

227-35

issue

1-2

eissn

0006-8993

issn

1872-6240

pii

S0006899399024464

journal_volume

856

pub_type

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