The DOI matches its Crossref record; 241 of the 245 references it cites were found in a registry or an index.
Nicotine and endogenous opioids: Neurochemical and pharmacological evidence
Abstract
Although the mesolimbic dopamine hypothesis is the most influential theory of nicotine reward and reinforcement, there has been a consensus that other neurotransmitter systems contribute to the addictive properties of nicotine as well. In this regard, the brain opioidergic system is of interest. Striatum is rich in opioid peptides and opioid receptors, and striatal opioidergic neurons are engaged in a bidirectional communication with midbrain dopaminergic neurons, closely regulating each other's activity. Enkephalins and dynorphins exert opposing actions on dopaminergic neurons, increasing and decreasing dopamine release respectively, and are components of circuits promoting positive or negative motivational and affective states. Moreover, dopamine controls the synthesis of striatal enkephalins and dynorphins. Evidence suggests that opioidergic function is altered after nicotine and endogenous opioids are involved in nicotine's behavioral effects. 1) The synthesis and release of β-endorphin, met-enkephalin and dynorphin in brain, especially nucleus accumbens (NAc), are altered after acute or chronic nicotine treatment and during nicotine withdrawal. 2) Although opioid receptor binding and mRNA do not appear to change in the striatum during nicotine withdrawal, the activity of κ-opioid (KOPr) and δ-opioid (DOPr) receptors is attenuated in NAc. 3) The nicotine withdrawal syndrome reminisces that of opiates, and naloxone precipitates some of its somatic, motivational, and affective signs. 4) Genetic and pharmacological studies indicate that μ-opioid (MOPr) receptors are mainly involved in nicotine reward, while DOPrs contribute to the emotional and KOPrs to the aversive responses of nicotine. 5) Finally, MOPrs and enkephalin, but not β-endorphin or dynorphin, are necessary for the physical manifestations of nicotine withdrawal. This article is part of a Special Issue entitled 'Trends in neuropharmacology: in memory of Erminio Costa'.
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“As nAChR activation affects the release of virtually every major neurotransmitter [106, 117, 118], chronic nicotine exposure is likely to cause global alterations in brain neurotransmission.”
From Mechanistic insights into nicotine withdrawal (2011) · cites this paper as [106]
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Metadata
- Authors
- Hadjiconstantinou, M., & Neff, N. H.
- Affiliations
- The Ohio State University (US)
- Corresponding author
- Hadjiconstantinou, Maria
- Venue
- Neuropharmacology
- Publisher
- Elsevier BV
- Published
- 2011-06
- Volume
- 60
- Issue
- 7-8
- Pages
- 1209-1220
- ISSN
- 0028-3908 (ISSN-L)
- OpenAlex
- W2076527782
- Cited by
- 81
- References
- 245
- Citations by year
- 2025: 3 · 2024: 3 · 2023: 1 · 2022: 2 · 2021: 5 · 2020: 6 · 2019: 4 · 2018: 6 · 2017: 7 · 2016: 6 · 2015: 11 · 2014: 9 · 2013: 5 · 2012: 11
- FWCI
- 0.52
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- Locations
- Neuropharmacology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuropeptides and Animal Physiology
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nicotinic Acetylcholine Receptors Study
- Keywords
- nicotine, endogenous opioids, nicotine reward, nicotine withdrawal, nucleus accumbens, striatum, dopamine, opioid receptors, mu-opioid receptor, kappa opioid receptor, delta opioid receptor, enkephalin, dynorphin, beta-endorphin, mesolimbic dopamine system, nicotine dependence
- MeSH terms
- Animals, Nicotine, Nucleus Accumbens, Receptors, Nicotinic, Substance Withdrawal Syndrome, Neurotransmitter Agents, Dopamine Agonists, Nicotinic Agonists, Opioid Peptides, Mice, Rats
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