Morphine intake and the effects of naltrexone and buprenorphine on the acquisition of methamphetamine intake

E. C. Eastwood, Tamara Phillips

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

Some common genetic factors appear to influence risk for drug dependence across multiple drugs of abuse. In previous research, mice that were selectively bred for higher amounts of methamphetamine consumption, using a two-bottle choice methamphetamine drinking procedure, were found to be less sensitive to the locomotor stimulant effects of morphine and of the more selective μ-opioid receptor agonist fentanyl, compared to mice that were bred for low methamphetamine consumption. This suggested that μ-opioid receptor-mediated pathways may influence genetic risk for methamphetamine consumption. We hypothesized that these differences in opioid sensitivity would impact opioid intake in the methamphetamine drinking lines and that drugs with μ-opioid receptor activity would impact methamphetamine intake. Consumption of morphine was examined in 2, two-bottle choice studies, one that compared morphine to quinine consumption and another that used a saccharin fading procedure. Next, naltrexone (0, 0.5, 1, 2, 5, 10 and 20mg/kg), a μ-opioid receptor antagonist, and buprenorphine (0, 1, 2 or 4mg/kg), a μ-opioid receptor partial agonist, were each examined for their effects on the acquisition of methamphetamine consumption. Low methamphetamine drinking mice consumed more morphine compared to high methamphetamine drinking mice. Naltrexone did not alter methamphetamine consumption in either selected line; however, buprenorphine reduced methamphetamine intake in the high methamphetamine drinking line. These data show that greater sensitivity to opioids is associated with greater opioid intake and warrant further investigation of drugs with μ-opioid receptor-specific agonist activity in genetically determined differences in methamphetamine consumption.

Original languageEnglish (US)
Pages (from-to)226-235
Number of pages10
JournalGenes, Brain and Behavior
Volume13
Issue number2
DOIs
StatePublished - Feb 2014

Fingerprint

Buprenorphine
Naltrexone
Methamphetamine
Morphine
Opioid Receptors
Drinking
Opioid Analgesics
Saccharin
Quinine
Narcotic Antagonists
Street Drugs
Fentanyl
Pharmaceutical Preparations
Substance-Related Disorders

Keywords

  • μ-Opioid receptor
  • Addiction
  • Amphetamine
  • Opioid
  • Psychostimulant
  • Quinine
  • Reward
  • Saccharin
  • Selective breeding
  • Two-bottle choice drinking

ASJC Scopus subject areas

  • Behavioral Neuroscience
  • Genetics
  • Neurology

Cite this

Morphine intake and the effects of naltrexone and buprenorphine on the acquisition of methamphetamine intake. / Eastwood, E. C.; Phillips, Tamara.

In: Genes, Brain and Behavior, Vol. 13, No. 2, 02.2014, p. 226-235.

Research output: Contribution to journalArticle

@article{210ebdc878b246c2b6b59654ba94ab61,
title = "Morphine intake and the effects of naltrexone and buprenorphine on the acquisition of methamphetamine intake",
abstract = "Some common genetic factors appear to influence risk for drug dependence across multiple drugs of abuse. In previous research, mice that were selectively bred for higher amounts of methamphetamine consumption, using a two-bottle choice methamphetamine drinking procedure, were found to be less sensitive to the locomotor stimulant effects of morphine and of the more selective μ-opioid receptor agonist fentanyl, compared to mice that were bred for low methamphetamine consumption. This suggested that μ-opioid receptor-mediated pathways may influence genetic risk for methamphetamine consumption. We hypothesized that these differences in opioid sensitivity would impact opioid intake in the methamphetamine drinking lines and that drugs with μ-opioid receptor activity would impact methamphetamine intake. Consumption of morphine was examined in 2, two-bottle choice studies, one that compared morphine to quinine consumption and another that used a saccharin fading procedure. Next, naltrexone (0, 0.5, 1, 2, 5, 10 and 20mg/kg), a μ-opioid receptor antagonist, and buprenorphine (0, 1, 2 or 4mg/kg), a μ-opioid receptor partial agonist, were each examined for their effects on the acquisition of methamphetamine consumption. Low methamphetamine drinking mice consumed more morphine compared to high methamphetamine drinking mice. Naltrexone did not alter methamphetamine consumption in either selected line; however, buprenorphine reduced methamphetamine intake in the high methamphetamine drinking line. These data show that greater sensitivity to opioids is associated with greater opioid intake and warrant further investigation of drugs with μ-opioid receptor-specific agonist activity in genetically determined differences in methamphetamine consumption.",
keywords = "μ-Opioid receptor, Addiction, Amphetamine, Opioid, Psychostimulant, Quinine, Reward, Saccharin, Selective breeding, Two-bottle choice drinking",
author = "Eastwood, {E. C.} and Tamara Phillips",
year = "2014",
month = "2",
doi = "10.1111/gbb.12100",
language = "English (US)",
volume = "13",
pages = "226--235",
journal = "Genes, Brain and Behavior",
issn = "1601-1848",
publisher = "Wiley-Blackwell",
number = "2",

}

TY - JOUR

T1 - Morphine intake and the effects of naltrexone and buprenorphine on the acquisition of methamphetamine intake

AU - Eastwood, E. C.

AU - Phillips, Tamara

PY - 2014/2

Y1 - 2014/2

N2 - Some common genetic factors appear to influence risk for drug dependence across multiple drugs of abuse. In previous research, mice that were selectively bred for higher amounts of methamphetamine consumption, using a two-bottle choice methamphetamine drinking procedure, were found to be less sensitive to the locomotor stimulant effects of morphine and of the more selective μ-opioid receptor agonist fentanyl, compared to mice that were bred for low methamphetamine consumption. This suggested that μ-opioid receptor-mediated pathways may influence genetic risk for methamphetamine consumption. We hypothesized that these differences in opioid sensitivity would impact opioid intake in the methamphetamine drinking lines and that drugs with μ-opioid receptor activity would impact methamphetamine intake. Consumption of morphine was examined in 2, two-bottle choice studies, one that compared morphine to quinine consumption and another that used a saccharin fading procedure. Next, naltrexone (0, 0.5, 1, 2, 5, 10 and 20mg/kg), a μ-opioid receptor antagonist, and buprenorphine (0, 1, 2 or 4mg/kg), a μ-opioid receptor partial agonist, were each examined for their effects on the acquisition of methamphetamine consumption. Low methamphetamine drinking mice consumed more morphine compared to high methamphetamine drinking mice. Naltrexone did not alter methamphetamine consumption in either selected line; however, buprenorphine reduced methamphetamine intake in the high methamphetamine drinking line. These data show that greater sensitivity to opioids is associated with greater opioid intake and warrant further investigation of drugs with μ-opioid receptor-specific agonist activity in genetically determined differences in methamphetamine consumption.

AB - Some common genetic factors appear to influence risk for drug dependence across multiple drugs of abuse. In previous research, mice that were selectively bred for higher amounts of methamphetamine consumption, using a two-bottle choice methamphetamine drinking procedure, were found to be less sensitive to the locomotor stimulant effects of morphine and of the more selective μ-opioid receptor agonist fentanyl, compared to mice that were bred for low methamphetamine consumption. This suggested that μ-opioid receptor-mediated pathways may influence genetic risk for methamphetamine consumption. We hypothesized that these differences in opioid sensitivity would impact opioid intake in the methamphetamine drinking lines and that drugs with μ-opioid receptor activity would impact methamphetamine intake. Consumption of morphine was examined in 2, two-bottle choice studies, one that compared morphine to quinine consumption and another that used a saccharin fading procedure. Next, naltrexone (0, 0.5, 1, 2, 5, 10 and 20mg/kg), a μ-opioid receptor antagonist, and buprenorphine (0, 1, 2 or 4mg/kg), a μ-opioid receptor partial agonist, were each examined for their effects on the acquisition of methamphetamine consumption. Low methamphetamine drinking mice consumed more morphine compared to high methamphetamine drinking mice. Naltrexone did not alter methamphetamine consumption in either selected line; however, buprenorphine reduced methamphetamine intake in the high methamphetamine drinking line. These data show that greater sensitivity to opioids is associated with greater opioid intake and warrant further investigation of drugs with μ-opioid receptor-specific agonist activity in genetically determined differences in methamphetamine consumption.

KW - μ-Opioid receptor

KW - Addiction

KW - Amphetamine

KW - Opioid

KW - Psychostimulant

KW - Quinine

KW - Reward

KW - Saccharin

KW - Selective breeding

KW - Two-bottle choice drinking

UR - http://www.scopus.com/inward/record.url?scp=84893014536&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84893014536&partnerID=8YFLogxK

U2 - 10.1111/gbb.12100

DO - 10.1111/gbb.12100

M3 - Article

VL - 13

SP - 226

EP - 235

JO - Genes, Brain and Behavior

JF - Genes, Brain and Behavior

SN - 1601-1848

IS - 2

ER -