Influence of morphine, β-endorphin and naloxone on the synthesis of phosphoinositides in the rat midbrain

R. Natsuki, Robert Hitzemann, H. H. Loh

Research output: Contribution to journalArticle

4 Citations (Scopus)

Abstract

The effect of morphine, β-endorphin and naloxone on the initial incorporation of 32Pi and [3H]glycerol into TPI, DPI and PI were measured in discrete subcellular fractions of the rat midbrain. Morphine and β-endorphin significantly increased microsomal 32Pi incorporation into TPI and PI but not DPI. Although neither morphine nor β-endorphin significantly affected the levels of [3H]TPI or [3H]DPI, both agents significantly increased [3H]PI levels. All of the significant effects induced by morphine were blocked by naloxone treatment and were decreased after chronic morphine administration. However, naloxone treatment alone also mimicked all the effects of morphine except the increased incorporation of [3H]glycerol into PI. It was also found that chronic morphine treatment significantly increased the incorporation of 32Pi into synaptic TPI and DPI. This effect, however, did not show regional specificity being found in both cortical and subcortical synaptic membranes. Overall, the results suggest that the mechanisms of opioid action are closely associated with changes in the turnover of the brain phosphoinositides.

Original languageEnglish (US)
Pages (from-to)233-250
Number of pages18
JournalResearch Communications in Chemical Pathology and Pharmacology
Volume24
Issue number2
StatePublished - 1979
Externally publishedYes

Fingerprint

Endorphins
Naloxone
Mesencephalon
Phosphatidylinositols
Morphine
Rats
Glycerol
Synaptic Membranes
Subcellular Fractions
Opioid Analgesics
Brain
Membranes

ASJC Scopus subject areas

  • Pharmacology
  • Toxicology

Cite this

@article{07edcd9df2b04fd5a156710722267901,
title = "Influence of morphine, β-endorphin and naloxone on the synthesis of phosphoinositides in the rat midbrain",
abstract = "The effect of morphine, β-endorphin and naloxone on the initial incorporation of 32Pi and [3H]glycerol into TPI, DPI and PI were measured in discrete subcellular fractions of the rat midbrain. Morphine and β-endorphin significantly increased microsomal 32Pi incorporation into TPI and PI but not DPI. Although neither morphine nor β-endorphin significantly affected the levels of [3H]TPI or [3H]DPI, both agents significantly increased [3H]PI levels. All of the significant effects induced by morphine were blocked by naloxone treatment and were decreased after chronic morphine administration. However, naloxone treatment alone also mimicked all the effects of morphine except the increased incorporation of [3H]glycerol into PI. It was also found that chronic morphine treatment significantly increased the incorporation of 32Pi into synaptic TPI and DPI. This effect, however, did not show regional specificity being found in both cortical and subcortical synaptic membranes. Overall, the results suggest that the mechanisms of opioid action are closely associated with changes in the turnover of the brain phosphoinositides.",
author = "R. Natsuki and Robert Hitzemann and Loh, {H. H.}",
year = "1979",
language = "English (US)",
volume = "24",
pages = "233--250",
journal = "Research Communications in Molecular Pathology and Pharmacology",
issn = "0034-5164",
publisher = "PJD Publications Ltd",
number = "2",

}

TY - JOUR

T1 - Influence of morphine, β-endorphin and naloxone on the synthesis of phosphoinositides in the rat midbrain

AU - Natsuki, R.

AU - Hitzemann, Robert

AU - Loh, H. H.

PY - 1979

Y1 - 1979

N2 - The effect of morphine, β-endorphin and naloxone on the initial incorporation of 32Pi and [3H]glycerol into TPI, DPI and PI were measured in discrete subcellular fractions of the rat midbrain. Morphine and β-endorphin significantly increased microsomal 32Pi incorporation into TPI and PI but not DPI. Although neither morphine nor β-endorphin significantly affected the levels of [3H]TPI or [3H]DPI, both agents significantly increased [3H]PI levels. All of the significant effects induced by morphine were blocked by naloxone treatment and were decreased after chronic morphine administration. However, naloxone treatment alone also mimicked all the effects of morphine except the increased incorporation of [3H]glycerol into PI. It was also found that chronic morphine treatment significantly increased the incorporation of 32Pi into synaptic TPI and DPI. This effect, however, did not show regional specificity being found in both cortical and subcortical synaptic membranes. Overall, the results suggest that the mechanisms of opioid action are closely associated with changes in the turnover of the brain phosphoinositides.

AB - The effect of morphine, β-endorphin and naloxone on the initial incorporation of 32Pi and [3H]glycerol into TPI, DPI and PI were measured in discrete subcellular fractions of the rat midbrain. Morphine and β-endorphin significantly increased microsomal 32Pi incorporation into TPI and PI but not DPI. Although neither morphine nor β-endorphin significantly affected the levels of [3H]TPI or [3H]DPI, both agents significantly increased [3H]PI levels. All of the significant effects induced by morphine were blocked by naloxone treatment and were decreased after chronic morphine administration. However, naloxone treatment alone also mimicked all the effects of morphine except the increased incorporation of [3H]glycerol into PI. It was also found that chronic morphine treatment significantly increased the incorporation of 32Pi into synaptic TPI and DPI. This effect, however, did not show regional specificity being found in both cortical and subcortical synaptic membranes. Overall, the results suggest that the mechanisms of opioid action are closely associated with changes in the turnover of the brain phosphoinositides.

UR - http://www.scopus.com/inward/record.url?scp=0018748211&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0018748211&partnerID=8YFLogxK

M3 - Article

VL - 24

SP - 233

EP - 250

JO - Research Communications in Molecular Pathology and Pharmacology

JF - Research Communications in Molecular Pathology and Pharmacology

SN - 0034-5164

IS - 2

ER -