ArticleThe European journal of neuroscience2016
Amphetamine elevates nucleus accumbens dopamine via an action potential-dependent mechanism that is modulated by endocannabinoids.
Article in The European journal of neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 45 citations in OpenAlex.
- Cannabinoid-based Pharmacology for the Management of Substance Use Disorders.Current topics in behavioral neurosciences · 2026Review
- The use ofFrontiers in cell and developmental biology · 2026Review
- G protein-coupled receptor modulation of striatal dopamine transmission: Implications for psychoactive drug effects.British journal of pharmacology · 2024Review
- Repeated chemogenetic activation of dopaminergic neurons induces reversible changes in baseline and amphetamine-induced behaviors.Psychopharmacology · 2023Article
- Review
- ABHD6 Controls Amphetamine-Stimulated Hyperlocomotion: Involvement of CBCannabis and cannabinoid research · 2022Article
- Viloxazine for the Treatment of Attention Deficit Hyperactivity Disorder.Health psychology research · 2022Article
- Cocaine-induced increases in motivation require 2-arachidonoylglycerol mobilization and CB1 receptor activation in the ventral tegmental area.Neuropharmacology · 2021Article
- Modulating the Neuromodulators: Dopamine, Serotonin, and the Endocannabinoid System.Trends in neurosciences · 2021Review
- D2 Receptors in the Periaqueductal Gray/Dorsal Raphe Modulate Peripheral Inflammatory Hyperalgesia via the Rostral Ventral Medulla.Neuroscience · 2021Article
- Restraint Stress Potentiated Morphine Sensitization: Involvement of Dopamine Receptors within the Nucleus Accumbens.Neurochemical research · 2021Article
- A Brain on Cannabinoids: The Role of Dopamine Release in Reward Seeking and Addiction.Cold Spring Harbor perspectives in medicine · 2021Review
- Selenoprotein P Modulates Methamphetamine Enhancement of Vesicular Dopamine Release in Mouse Nucleus Accumbens Via Dopamine D2 Receptors.Frontiers in neuroscience · 2021Article
- Exercise intervention can reduce the degree of drug dependence of patients with amphetamines/addiction by improving dopamine level and immunity and reducing negative emotions.American journal of translational research · 2021Article
- Spiking and Membrane Properties of Rat Olfactory Bulb Dopamine Neurons.Frontiers in cellular neuroscience · 2020Article
- The novel MAGL inhibitor MJN110 enhances responding to reward-predictive incentive cues by activation of CB1 receptors.Neuropharmacology · 2020Article
- Central GLP-1 receptors: Novel molecular targets for cocaine use disorder.Physiology & behavior · 2019Review
- Electrochemistry at the Synapse.Annual review of analytical chemistry (Palo Alto, Calif.) · 2019Review
- Dopaminergic basis for signaling belief updates, but not surprise, and the link to paranoia.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Inhibition of endocannabinoid degradation rectifies motivational and dopaminergic deficits in the Q175 mouse model of Huntington's disease.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2018Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
The reinforcing effects of abused drugs are mediated by their ability to elevate nucleus accumbens dopamine. Amphetamine (AMPH) was historically thought to increase dopamine by an action potential-independent, non-exocytotic type of release called efflux, involving reversal of dopamine transporter function and driven by vesicular dopamine depletion. Growing evidence suggests that AMPH also acts by an action potential-dependent mechanism. Indeed, fast-scan cyclic voltammetry demonstrates that AMPH activates dopamine transients, reward-related phasic signals generated by burst firing of dopamine neurons and dependent on intact vesicular dopamine. Not established for AMPH but indicating a shared mechanism, endocannabinoids facilitate this activation of dopamine transients by broad classes of abused drugs. Here, using fast-scan cyclic voltammetry coupled to pharmacological manipulations in awake rats, we investigated the action potential and endocannabinoid dependence of AMPH-induced elevations in nucleus accumbens dopamine. AMPH increased the frequency, amplitude and duration of transients, which were observed riding on top of slower dopamine increases. Surprisingly, silencing dopamine neuron firing abolished all AMPH-induced dopamine elevations, identifying an action potential-dependent origin. Blocking cannabinoid type 1 receptors prevented AMPH from increasing transient frequency, similar to reported effects on other abused drugs, but not from increasing transient duration and inhibiting dopamine uptake. Thus, AMPH elevates nucleus accumbens dopamine by eliciting transients via cannabinoid type 1 receptors and promoting the summation of temporally coincident transients, made more numerous, larger and wider by AMPH. Collectively, these findings are inconsistent with AMPH eliciting action potential-independent dopamine efflux and vesicular dopamine depletion, and support endocannabinoids facilitating phasic dopamine signalling as a common action in drug reinforcement.
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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.