Nicotine's opioid and anti-opioid interactions: Proposed role in smoking behavior

Aceto, Mario D.; Scates, Susan M.; Ji, Zhen; Bowman, Edward R.

doi:10.1016/0926-6917(93)90009-f

Cited by 22 publications

(25 citation statements)

References 9 publications

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“…Subsequent human clinical trials with naloxone or the longer acting opioid receptor antagonist naltrexone showed inconsistent results both in the degree that these agents diminished tobacco smoking as well as on their behavioral effects (Nemeth-Coslett and Griffiths, 1986;Gorelick et al, 1988;Sutherland et al, 1995;Wewers et al, 1999). Aceto et al (1993) examining the analgesic effects of nicotine in rodents, and Pomerleau (1998) in a review of both human and animal data, postulated that nicotine produced both pro-and antiopioidergic effects. These were further confounded by the complexity of this neurotransmitter system and its possible involvement in both reinforcing and withdrawal phenomena.…”

Section: Introductionmentioning

confidence: 99%

Smoking Modulation of μ-Opioid and Dopamine D2 Receptor-Mediated Neurotransmission in Humans

Scott

Domino

Heitzeg

et al. 2006

Neuropsychopharmacol

112

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This is a pilot examination of the hypothesis that some of the effects of smoking cigarettes in humans are mediated through nicotine activation of opioid and dopamine (DA) neurotransmission. Neuroimaging was performed using positron emission tomography and the radiotracers [11 C]carfentanil and [ 11 C]raclopride, labeling m-opioid and DA D2 receptors, respectively. Six healthy male smokers were abstinent overnight. After radiotracer administration, subjects smoked two denicotinized cigarettes, followed 45 min later by two average nicotine cigarettes. Dynamic data were acquired over 90 min, and transformed into parametric maps of receptor availability in vivo (binding potential, BP), corresponding to low and high nicotine smoking periods and analyzed on a voxel-by-voxel basis using SPM'99 and correction for multiple comparisons. Significant activation of m-opioid receptor-mediated neurotransmission from denicotinized to average nicotine conditions was observed in the right anterior cingulate cortex. DA D2 neurotransmission was activated in the ventral basal ganglia, correlating with Fagerströ m scale nicotine dependence scores. Lower m-opioid receptor BP was also detected during the denicotinized smoking condition in the smoker group, compared to baseline scans in non-smokers, in the cingulate cortex, thalamus, ventral basal ganglia, and amygdala. These reductions were reversed during the average nicotine condition in the thalamus, ventral basal ganglia and amygdala. These data point to both the feasibility of simultaneously examining opioid and DA neurotransmission responses to smoking in humans, as well as to the need to examine non-nicotine aspects of smoking to more fully understand the behavioral effects of this drug.

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Section: Introductionmentioning

confidence: 99%

Smoking Modulation of μ-Opioid and Dopamine D2 Receptor-Mediated Neurotransmission in Humans

Scott

Domino

Heitzeg

et al. 2006

Neuropsychopharmacol

112

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“…Al though endogenous opioid systems may be involved in nico tine-induced antinociception in mice (3,26) and dogs (12), there is little evidence to suggest opioid involvement in rats. Rats pretreated with the opiate antagonist naloxone SC still exhib ited antinociception after either SC or suhcortical nicotine in jection (11,(24)(25)(26).…”

mentioning

confidence: 99%

The Analgesia-Enhancing Component of Ingested Amniotic Fluid Does Not Affect Nicotine-Induced Antinociception in Naltrexone-Treated Rats

Robinson-Vanderwerf

Pirro

Caggiula

et al. 1997

Pharmacology Biochemistry and Behavior

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PHA RM ACOL BlOCH FM HEHA Y 511( I) 147-15 I. IlJ'I7.-lngestion of ;1I1111iotic fluid and placenta by rats h;ls been shown to enh;lllce opioid-mediated ,Intinociception but not arrect the nonopioid-mediated antinociception pl'llduced bv aspirin. su~ csting spccificity for opioid-mediated proccsses. Ilowcver. enhanccment hy the active substancc(s) in amniotic fluid and pia cc'nta (POEF. for placental o[Jioid-enhancing factor) of antinociception produced bv other nonopioidmech,lllisms 1m.. yet to be examine'll. Thc present experiments tested whether ingestion of amniotic fluid enlwnees thc antinociecption produced by nicotine injection. In ExperimLOnt I A. LOnhancelllent of morphine-mediated antinociception by ingestionl>f amniotic fluid W;h den]()nstrared in ,I hot-plate assay. In Experiment I B. rats prdreated with naltrexone werc given an orogastric infusion of amniotic fluid m contl'lll (0.25 ml). then injected with nicotine (0.0.075.0.125, or 0.225 mglkg subcut'lncously). then tested for antinocicc'ption in a hot-pl;lte 'ISS;ly. Amniotic fluid ingestion did not enhance the antinociccption produccd by v;nious doscs of nicotinLO. In Expcrimcnt 2. rats pretrcated with naltrcxone were given an orogaslric infusion of amniotic fluid (0.0.125. 11.25. or 0.50 ml) ;\Ild then injcctcd with n.125 m~lk~ nicotinc. None of the doscs of amniotic fluid enhanced thc nicotinc induccd <1n1 inocicept ion. Thc'findings of these expcr;'illents lend support 10 our contcntion that thc enhancemcnt bv POEF of

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“…Pretreatment with the kappa opioid agonists U50488 and TRK-820 attenuated mecamylamine precipitated withdrawal symptoms in nicotinedependent rats (Ise et al, 2002). Aceto et al (1993) reviewed the literature to that date and proposed an opioid role in smoking. Pomerleau's review (1998) further summarized findings of smoking and the role of endogenous opioids to that date.…”

Section: Nicotine/tobacco Smoking and Brain Opioid Peptidesmentioning

confidence: 99%

“…In rodents the administration of the opioid antagonist naloxone decreases nicotine-induced antinociception (Aceto et al, 1993;Campbell et al, 2006;Tripathi et al, 1982;Zarrindast et al, 1997). In addition, nicotine administration prior to the central administration of betafunaltrexamine (β-FNA), an irreversible mu opioid receptor antagonist, attenuated β-FNA antagonism of morphine induced antinociception, indicating that nicotine administration led to endogenous opioid peptide release, which activated mu opioid receptors and blocked β-FNA's effect (Davenport et al, 1990).…”

Section: Direct Involvement Of the Endogenous Opioid System In The Acmentioning

confidence: 99%

Tobacco/nicotine and endogenous brain opioids

Xue

Domino

2008

Progress in Neuro-Psychopharmacology and Biological Psychiatry

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Smoking is a major public health problem with devastating health consequences. Although many cigarette smokers are able to quit, equal numbers of others cannot! Standard medications to assist in smoking cessation, such as nicotine replacement therapies and bupropion, are ineffective in many remaining smokers. Recent developments in the neurobiology of nicotine dependence have identified several neurotransmitter systems that may contribute to the process of smoking maintenance and relapse. These include: especially dopamine, but also norepinephrine, 5-hydroxytryptamine, acetylcholine, endogenous opioids, gamma-aminobutyric acid (GABA), glutamate, and endocannabinoids. The present review examines the limited contribution of the endogenous opioid system to the complex effects of nicotine/tobacco smoking.

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Nicotine's opioid and anti-opioid interactions: Proposed role in smoking behavior

Cited by 22 publications

References 9 publications

Smoking Modulation of μ-Opioid and Dopamine D2 Receptor-Mediated Neurotransmission in Humans

Smoking Modulation of μ-Opioid and Dopamine D2 Receptor-Mediated Neurotransmission in Humans

The Analgesia-Enhancing Component of Ingested Amniotic Fluid Does Not Affect Nicotine-Induced Antinociception in Naltrexone-Treated Rats

Tobacco/nicotine and endogenous brain opioids

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