ArticleNature neuroscience2013
Reducing cannabinoid abuse and preventing relapse by enhancing endogenous brain levels of kynurenic acid.
Article in Nature neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
60 citing papers in PubMed, 96 citations in OpenAlex.
- Effects of nicotinic receptor antagonism on nicotine and THC self-administration in a model of polysubstance use.The international journal of neuropsychopharmacology · 2026Article
- Pharmacokinetics of oral Δ9-tetrahydrocannabinol (THC) administration in vervet monkeys.Journal of cannabis research · 2026Article
- The role of the kynurenine pathway in conditioned place aversion induced by synthetic cannabinoid CP-55940.Behavioral and brain functions : BBF · 2026Article
- The need to incorporate polysubstance use in neuropsychopharmacology research: Biological lessons and new opportunities.Addiction neuroscience · 2026Article
- Individual and additive effects of childhood maltreatment and substance use disorder histories on baseline and stress-induced changes in peripheral stress biomarkers.Psychopharmacology · 2026Article
- Effects of nicotinic receptor antagonism on nicotine and THC self-administration in a model of polysubstance use.bioRxiv : the preprint server for biology · 2025Article
- Chronic ΔNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2025Article
- The kynurenine pathway as a potential link between ethanol-induced behavioral alterations and neuroinflammation.Frontiers in pharmacology · 2025Article
- Impact of Substance Use Disorder on Tryptophan Metabolism Through the Kynurenine Pathway: A Narrative Review.Metabolites · 2024Review
- Neuroactive Kynurenines as Pharmacological Targets: New Experimental Tools and Exciting Therapeutic Opportunities.Pharmacological reviews · 2024Review
- Cannabis use disorder: from neurobiology to treatment.The Journal of clinical investigation · 2024Review
- Long-term disruption of tissue levels of glutamate and glutamatergic neurotransmission neuromodulators, taurine and kynurenic acid induced by amphetamine.Psychopharmacology · 2024Article
- Cannabinoids and monoaminergic system: implications for learning and memory.Frontiers in neuroscience · 2024Review
- Review
- Targeting corticostriatal transmission for the treatment of cannabinoid use disorder.Trends in pharmacological sciences · 2023Review
- Tryptophan and Substance Abuse: Mechanisms and Impact.International journal of molecular sciences · 2023Review
- Influx of kynurenine into the brain is involved in the reduction of ethanol consumption induced by Ro 61-8048 after chronic intermittent ethanol in mice.British journal of pharmacology · 2022Article
- Article
- Negative and positive allosteric modulators of the α7 nicotinic acetylcholine receptor regulates the ability of adolescent binge alcohol exposure to enhance adult alcohol consumption.Frontiers in behavioral neuroscience · 2022Article
- Alterations in rat prefrontal cortex kynurenic acid levels are involved in the enduring cognitive dysfunctions induced by tetrahydrocannabinol exposure during the adolescence.Frontiers in psychiatry · 2022Article
Corrections and comments
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Authors and funding
19 authors at 6 institutions in 3 countries.
Funding
Abstract
In the reward circuitry of the brain, α-7-nicotinic acetylcholine receptors (α7nAChRs) modulate effects of Δ(9)-tetrahydrocannabinol (THC), marijuana's main psychoactive ingredient. Kynurenic acid (KYNA) is an endogenous negative allosteric modulator of α7nAChRs. Here we report that the kynurenine 3-monooxygenase (KMO) inhibitor Ro 61-8048 increases brain KYNA levels and attenuates cannabinoid-induced increases in extracellular dopamine in reward-related brain areas. In the self-administration model of drug abuse, Ro 61-8048 reduced the rewarding effects of THC and the synthetic cannabinoid WIN 55,212-2 in squirrel monkeys and rats, respectively, and it also prevented relapse to drug-seeking induced by reexposure to cannabinoids or cannabinoid-associated cues. The effects of enhancing endogenous KYNA levels with Ro 61-8048 were prevented by positive allosteric modulators of α7nAChRs. Despite a clear need, there are no medications approved for treatment of marijuana dependence. Modulation of KYNA offers a pharmacological strategy for achieving abstinence from marijuana and preventing relapse.
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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.