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Cited by 581

The DOI matches its Crossref record; 31 of the 31 references it cites were found in a registry or an index.

How Addictive Drugs Disrupt Presynaptic Dopamine Neurotransmission

Open access
Sulzer, David·2011·Neuron

Abstract

The fundamental principle that unites addictive drugs appears to be that each enhances synaptic dopamine by means that dissociate it from normal behavioral control, so that they act to reinforce their own acquisition. This occurs via the modulation of synaptic mechanisms involved in learning, including enhanced excitation or disinhibition of dopamine neuron activity, blockade of dopamine reuptake, and altering the state of the presynaptic terminal to enhance evoked over basal transmission. Amphetamines offer an exception to such modulation in that they combine multiple effects to produce non-exocytic stimulation-independent release of neurotransmitter via reverse transport independent from normal presynaptic function. Questions on the molecular actions of addictive drugs, prominently including the actions of alcohol and solvents, remain unresolved, but their ability to co-opt normal presynaptic functions helps to explain why treatment for addiction has been challenging.

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Crossref · 10.1016/j.neuron.2011.02.010

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Metadata

Authors
Sulzer, D.
Venue
Neuron
Publisher
Elsevier BV
Published
2011-02
Volume
69
Issue
4
Pages
628-649
ISSN
0896-6273 (ISSN-L)
OpenAlex
W2030852918
Cited by
581
References
31
FWCI
20.73
Type
journal article
Language
en
Open access
bronze

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CoChat. (2026). Citation check: How Addictive Drugs Disrupt Presynaptic Dopamine Neurotransmission. https://app.cochat.ai/papers/10.1016/j.neuron.2011.02.010
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Sulzer, D. (2011). How Addictive Drugs Disrupt Presynaptic Dopamine Neurotransmission. Neuron. https://doi.org/10.1016/j.neuron.2011.02.010

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.