ArticleNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology2012
Chronic Δ⁹-tetrahydrocannabinol exposure induces a sensitization of dopamine D₂/₃ receptors in the mesoaccumbens and nigrostriatal systems.
Article in Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 2 of them syntheses that pooled it.
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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
26 citing papers in PubMed, 2 syntheses or guidelines pooled it, 56 citations in OpenAlex.
- A systematic review of neuroimaging and acute cannabis exposure in age-of-risk for psychosis.Translational psychiatry · 2021Pooled it
- Are cannabis-using and non-using patients different groups? Towards understanding the neurobiology of cannabis use in psychotic disorders.Journal of psychopharmacology (Oxford, England) · 2018Pooled it
- Decreased dopamine brain reactivity in marijuana abusers is associated with negative emotionality and addiction severity.Proceedings of the National Academy of Sciences of the United States of America · 2014Trial
- The role of subcortical brain tissue iron as an indicator of dopamine neurophysiology in adolescent cannabis use.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026Article
- Why Is Clozapine Uniquely Effective in Treatment-Resistant Schizophrenia? A Review and Proposal.Biological psychiatry · 2026Review
- Psychotomimetic compensation versus sensitization.Pharmacology research & perspectives · 2024Review
- Article
- Electrophysiological and behavioral correlates of cannabis use disorder.Cognitive, affective & behavioral neuroscience · 2022Article
- Chronic ∆-9-tetrahydrocannabinol administration delays acquisition of schedule-induced drinking in rats and retains long-lasting effects.Psychopharmacology · 2022Article
- Effects of prenatal synthetic cannabinoid exposure on the cerebellum of adolescent rat offspring.Heliyon · 2021Article
- Chronic Exposure to WIN55,212-2 During Adolescence Alters Prefrontal Dopamine Turnover and Induces Sensorimotor Deficits in Adult Rats.Neurotoxicity research · 2020Article
- D3 dopamine receptors and a missense mutation of fatty acid amide hydrolase linked in mouse and men: implication for addiction.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2020Article
- Genetic Predisposition vs Individual-Specific Processes in the Association Between Psychotic-like Experiences and Cannabis Use.JAMA psychiatry · 2019Article
- Cannabinoid disruption of learning mechanisms involved in reward processing.Learning & memory (Cold Spring Harbor, N.Y.) · 2018Review
- Preclinical Studies of Cannabinoid Reward, Treatments for Cannabis Use Disorder, and Addiction-Related Effects of Cannabinoid Exposure.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2018Review
- Pros and Cons of Medical Cannabis use by People with Chronic Brain Disorders.Current neuropharmacology · 2017Review
- Salience attribution and its relationship to cannabis-induced psychotic symptoms.Psychological medicine · 2016Article
- The effects of ΔNature · 2016Review
- Traditional marijuana, high-potency cannabis and synthetic cannabinoids: increasing risk for psychosis.World psychiatry : official journal of the World Psychiatric Association (WPA) · 2016Article
- Cannabidiol Counteracts Amphetamine-Induced Neuronal and Behavioral Sensitization of the Mesolimbic Dopamine Pathway through a Novel mTOR/p70S6 Kinase Signaling Pathway.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Δ⁹-tetrahydrocannabinol (THC), through its action on cannabinoid type-1 receptor (CB₁R), is known to activate dopamine (DA) neurotransmission. Functional evidence of a direct antagonistic interaction between CB₁R and DA D₂-receptors (D₂R) suggests that D₂R may be an important target for the modulation of DA neurotransmission by THC. The current study evaluated, in rodents, the effects of chronic exposure to THC (1 mg/kg/day; 21 days) on D₂R and D₃R availabilities using the D₂R-prefering antagonist and the D₃R-preferring agonist radiotracers [¹⁸F]fallypride and [³H]-(+)-PHNO, respectively. At 24 h after the last THC dose, D₂R and D₃R densities were significantly increased in midbrain. In caudate/putamen (CPu), THC exposure was associated with increased densities of D₂R with no change in D₂R mRNA expression, whereas in nucleus accumbens (NAcc) both D₃R binding and mRNA levels were upregulated. These receptor changes, which were completely reversed in CPu but only partially reversed in NAcc and midbrain at 1 week after THC cessation, correlated with an increased functionality of D₂/₃R in vivo, based on findings of increased locomotor suppressive effect of a presynaptic dose and enhanced locomotor activation produced by a postsynaptic dose of quinpirole. Concomitantly, the observations of a decreased gene expression of tyrosine hydroxylase in midbrain together with a blunted psychomotor response to amphetamine concurred to indicate a diminished presynaptic DA function following THC. These findings indicate that the early period following THC treatment cessation is associated with altered presynaptic D₂/₃R controlling DA synthesis and release in midbrain, with the concurrent development of postsynaptic D₂/₃R supersensitivity in NAcc and CPu. Such D₂/₃R neuroadaptations may contribute to the reinforcing and habit-forming properties of THC.
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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.