ArticlePsychopharmacology2010
Nicotine withdrawal and kappa-opioid receptors.
Article in Psychopharmacology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 18 citations in OpenAlex.
- The influence of stress and social defeat on neurobiological reinforcement mechanisms across reward to withdrawal in nicotine addiction.Psychopharmacology · 2025Review
- Altered mRNA Levels of Stress-Related Peptides in Mouse Hippocampus and Caudate-Putamen in Withdrawal after Long-Term Intermittent Exposure to Tobacco Smoke or Electronic Cigarette Vapour.International journal of molecular sciences · 2021Article
- Article
- Endogenous opioid system: a promising target for future smoking cessation medications.Psychopharmacology · 2017Review
- The opioid receptors as targets for drug abuse medication.British journal of pharmacology · 2015Review
- Role of the kappa-opioid receptor system in stress-induced reinstatement of nicotine seeking in rats.Behavioural brain research · 2014Article
- Dynorphin--still an extraordinarily potent opioid peptide.Molecular pharmacology · 2013Review
- Dysregulation of kappa-opioid receptor systems by chronic nicotine modulate the nicotine withdrawal syndrome in an age-dependent manner.Psychopharmacology · 2012Article
- CREB involvement in the regulation of striatal prodynorphin by nicotine.Psychopharmacology · 2012Article
- Desensitization of δ-opioid receptors in nucleus accumbens during nicotine withdrawal.Psychopharmacology · 2011Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
rationaleThe synthesis and release of dynorphin are increased in the caudate/putamen (CPU) and nucleus accumbens (NAc) of nicotine-withdrawn mice, suggesting a role in the nicotine abstinence syndrome.
objectivesThis study aims to investigate the consequences of enhanced dynorphinergic activity on kappa-opioid receptor (KOPr) expression, coupling, and function in CPU and NAc following chronic nicotine administration and withdrawal.
methodsMice were injected with nicotine-free base 2 mg/kg, or saline, sc, four times daily for 14 days and experiments performed at 24, 48, and 72 h after drug discontinuation. KOPr binding and mRNA were evaluated by [(3)H]-U69,593 autoradiography and in situ hybridization. KOPr coupling and function were investigated by agonist (U69-593)-stimulated [(35)S]GTPgammaS binding autoradiography and inhibition of adenylyl cyclase activity.
resultsKOPr binding density and mRNA in CPU and NAc were unaltered during nicotine withdrawal; however, KPOr mRNA was increased in midbrain. U69,593-stimulated [(35)S]GTPgammaS binding was attenuated in both striatal regions, especially in NAc. In NAc shell and core, stimulated [(35)S]GTPgammaS binding was significantly decreased by 24 h and further declined over the 72 h observation period. In CPU, significant changes were observed only at 72 h. Basal adenylyl cyclase activity decreased early during nicotine withdrawal and recovered by 48 h. Stimulation with U69,593 failed to inhibit adenylyl cyclase activity at all times studied.
conclusionsThese observations suggest that KOPr coupling and function are impaired in NAc and CPU during nicotine withdrawal, and imply receptor desensitization. KOPr desensitization might be a mechanism to ameliorate aversive behavioral symptoms, as nicotine withdrawal evolves.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.