ArticlePsychopharmacology2007
The effects of buprenorphine on fentanyl withdrawal in rats.
Article in Psychopharmacology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 25 citations in OpenAlex.
- GABAergic neurons in the ventrolateral periaqueductal gray mediate fentanyl withdrawal and self-administration in mice.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026Article
- A historical perspective on clonidine as an alpha-2A receptor agonist in the treatment of addictive behaviors: Focus on opioid dependence.INNOSC theranostics & pharmacological sciences · 2024Article
- Lipophilic analogues of D-cysteine prevent and reverse physical dependence to fentanyl in male rats.Frontiers in pharmacology · 2023Article
- Opioid use disorder: current trends and potential treatments.Frontiers in public health · 2023Review
- Comparative benefits of social housing and buprenorphine on wheel running depressed by morphine withdrawal in rats.Psychopharmacology · 2021Article
- Neurological correlates of brain reward circuitry linked to opioid use disorder (OUD): Do homo sapiens acquire or have a reward deficiency syndrome?Journal of the neurological sciences · 2020Review
- Higher anhedonia during withdrawal from initial opioid exposure is protective against subsequent opioid self-administration in rats.Psychopharmacology · 2020Article
- Progress in agonist therapy for substance use disorders: Lessons learned from methadone and buprenorphine.Neuropharmacology · 2019Review
- Can the chronic administration of the combination of buprenorphine and naloxone block dopaminergic activity causing anti-reward and relapse potential?Molecular neurobiology · 2011Article
- Neurobiological substrates for the dark side of compulsivity in addiction.Neuropharmacology · 2009Review
- A role for brain stress systems in addiction.Neuron · 2008Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
rationaleFentanyl is a potent mu-opioid receptor agonist that is widely used for the treatment of severe chronic pain. Discontinuation of fentanyl administration has been shown to induce a negative emotional state.
objectivesThe aim of the present studies was to investigate the effects of the partial mu-opioid receptor agonist buprenorphine on the negative emotional state associated with precipitated and spontaneous fentanyl withdrawal in rats. MATERIALS AND
methodsFentanyl and saline were chronically administered via osmotic minipumps. A discrete-trial intracranial self-stimulation procedure was used to provide a measure of brain reward function. Somatic signs were recorded from a checklist of opioid abstinence signs.
resultsNaloxone induced a deficit in brain reward function in rats chronically treated with fentanyl. Buprenorphine dose-dependently prevented the naloxone-induced deficit in brain reward function. Discontinuation of fentanyl administration was also associated with a deficit in brain reward function. After explantation of the minipumps, the administration of buprenorphine induced a potentiation of brain reward function in the fentanyl-withdrawing rats, but did not affect brain reward function of saline-treated control rats. Buprenorphine prevented the somatic withdrawal signs associated with spontaneous fentanyl withdrawal and attenuated the somatic signs associated with precipitated fentanyl withdrawal.
conclusionsBuprenorphine prevents affective and somatic fentanyl withdrawal signs. Moreover, buprenorphine is rewarding in rats previously exposed to fentanyl, but not in opioid-naïve rats. This pattern of results suggests that buprenorphine may be an effective treatment for the anhedonic-state associated with fentanyl withdrawal, but further study of buprenorphine's abuse potential is warranted.
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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.