Influence of chronic opioid treatment on low Km GTPase activity in rat brain: Evidence for the involvement of G-proteins in opioid tolerance

Influence of chronic opioid treatment on low Km GTPase activity in rat brain: Evidence for the... To investigate G protein function during the initial state of opioid tolerance, low Km GTPase activity was measured following chronic treatment with morphine (μ agonist) and butorphanol (μ/δ/κ mixed agonist) in rats. Chronic opioid administration (20 mg/kg, IP) was performed once a day for 7 consecutive days. Under these conditions, antinociceptive tolerance to morphine but not butorphanol was developed. Chronic morphine treatment enhanced basal low Km GTPase activity in the pons/medulla, but not in the cortex and midbrain. On the other hand, chronic butorphanol treatment had no effect on basal low Km GTPase activity. These results suggest that chronic in vivo treatment of rats with μ agonists leads to an increase in the hydrolysis of GTP to GDP, by a basal low Km GTPase activity of G-proteins in the pons/medulla and that an enhancement of GTPase activity in this specific area may contribute to the development of antinociceptive tolerance to μ agonists. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Brain Research Bulletin Elsevier

Influence of chronic opioid treatment on low Km GTPase activity in rat brain: Evidence for the involvement of G-proteins in opioid tolerance

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Publisher
Elsevier
Copyright
Copyright © 1995 Elsevier Ltd
ISSN
0361-9230
eISSN
1873-2747
DOI
10.1016/0361-9230(95)02033-8
Publisher site
See Article on Publisher Site

Abstract

To investigate G protein function during the initial state of opioid tolerance, low Km GTPase activity was measured following chronic treatment with morphine (μ agonist) and butorphanol (μ/δ/κ mixed agonist) in rats. Chronic opioid administration (20 mg/kg, IP) was performed once a day for 7 consecutive days. Under these conditions, antinociceptive tolerance to morphine but not butorphanol was developed. Chronic morphine treatment enhanced basal low Km GTPase activity in the pons/medulla, but not in the cortex and midbrain. On the other hand, chronic butorphanol treatment had no effect on basal low Km GTPase activity. These results suggest that chronic in vivo treatment of rats with μ agonists leads to an increase in the hydrolysis of GTP to GDP, by a basal low Km GTPase activity of G-proteins in the pons/medulla and that an enhancement of GTPase activity in this specific area may contribute to the development of antinociceptive tolerance to μ agonists.

Journal

Brain Research BulletinElsevier

Published: Jan 1, 1995

References

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