ReviewBrain research2015
Chronic cocaine disrupts mesocortical learning mechanisms.
Review in Brain research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
16 citing papers in PubMed, 32 citations in OpenAlex.
- Withdrawal-Induced Delirium in Opioid Dependence: A Systematic Review.Brain sciences · 2025Review
- Escalated oxycodone self-administration is associated with expression of voltage gated and calcium activated potassium channels in the mesocorticolimbic system in rats.Frontiers in pharmacology · 2025Article
- Disrupted Circadian Rhythms and Substance Use Disorders: A Narrative Review.Clocks & sleep · 2024Review
- The Effect of Transcranial Direct Current Stimulation (tDCS) on Cocaine Addiction: A Narrative Review.Journal of clinical medicine · 2023Review
- Molecular genetics of cocaine use disorders in humans.Molecular psychiatry · 2022Review
- Effects of muscarinic MNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2020Article
- Cocaine self-administration differentially activates microglia in the mouse brain.Neuroscience letters · 2020Article
- Nicotine Addiction: Neurobiology and Mechanism.Journal of pharmacopuncture · 2020Review
- Methylphenidate for Attention-Deficit and Hyperactivity Disorder in Adult Patients With Substance Use Disorders: Good Clinical Practice.Frontiers in psychiatry · 2020Review
- Dynamic CRMP2 Regulation of CaV2.2 in the Prefrontal Cortex Contributes to the Reinstatement of Cocaine Seeking.Molecular neurobiology · 2020Article
- Sex Differences and the Role of Estradiol in Mesolimbic Reward Circuits and Vulnerability to Cocaine and Opiate Addiction.Frontiers in behavioral neuroscience · 2020Review
- Fatty acid binding protein deletion prevents stress-induced preference for cocaine and dampens stress-induced corticosterone levels.Synapse (New York, N.Y.) · 2018Article
- Restoration of Kv7 Channel-Mediated Inhibition Reduces Cued-Reinstatement of Cocaine Seeking.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Dopamine terminals from the ventral tegmental area gate intrinsic inhibition in the prefrontal cortex.Physiological reports · 2017Article
- The Role of Dopamine and Its Dysfunction as a Consequence of Oxidative Stress.Oxidative medicine and cellular longevity · 2016Review
- Differential Expression of FosB Proteins and Potential Target Genes in Select Brain Regions of Addiction and Depression Patients.PloS one · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The addictive power of drugs of abuse such as cocaine comes from their ability to hijack natural reward and plasticity mechanisms mediated by dopamine signaling in the brain. Reward learning involves burst firing of midbrain dopamine neurons in response to rewards and cues predictive of reward. The resulting release of dopamine in terminal regions is thought to act as a teaching signaling to areas such as the prefrontal cortex and striatum. In this review, we posit that a pool of extrasynaptic dopaminergic D1-like receptors activated in response to dopamine neuron burst firing serve to enable synaptic plasticity in the prefrontal cortex in response to rewards and their cues. We propose that disruptions in these mechanisms following chronic cocaine use contribute to addiction pathology, in part due to the unique architecture of the mesocortical pathway. By blocking dopamine reuptake in the cortex, cocaine elevates dopamine signaling at these extrasynaptic receptors, prolonging D1-receptor activation and the subsequent activation of intracellular signaling cascades, and thus inducing long-lasting maladaptive plasticity. These cellular adaptations may account for many of the changes in cortical function observed in drug addicts, including an enduring vulnerability to relapse. Therefore, understanding and targeting these neuroadaptations may provide cognitive benefits and help prevent relapse in human drug addicts.
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What OpenQuestion holds
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.