Drugs of Abuse and Stress Trigger a Common Synaptic Adaptation in Dopamine Neurons

Drug seeking and drug self-administration in both animals and humans can be triggered by drugs of abuse themselves or by stressful events. Here, we demonstrate that in vivo administration of drugs of abuse with different molecular mechanisms of action as well as acute stress both increase strength a...

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Bibliographic Details
Published in:Neuron (Cambridge, Mass.) Mass.), 2003-02, Vol.37 (4), p.577-582
Main Authors: Saal, Daniel, Dong, Yan, Bonci, Antonello, Malenka, Robert C
Format: Article
Language:English
Subjects:
Adaptation, Physiological - drug effects
Adaptation, Physiological - physiology
Animals
Bipolar disorder
Brain
Cocaine
Dopamine
Dopamine - metabolism
Ethanol
Excitatory Postsynaptic Potentials - drug effects
Excitatory Postsynaptic Potentials - physiology
Experiments
In Vitro Techniques
Mice
Mice, Inbred C57BL
Mifepristone - pharmacology
Neuronal Plasticity - drug effects
Neuronal Plasticity - physiology
Neurons
Neurons - drug effects
Neurons - metabolism
Nicotine
Patch-Clamp Techniques
Receptors, AMPA - metabolism
Receptors, Glucocorticoid - antagonists & inhibitors
Receptors, Glucocorticoid - metabolism
Receptors, N-Methyl-D-Aspartate - metabolism
Rodents
Street Drugs - pharmacology
Stress, Physiological - physiopathology
Substance-Related Disorders - etiology
Substance-Related Disorders - metabolism
Synapses - metabolism
Ventral Tegmental Area - drug effects
Ventral Tegmental Area - metabolism
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Description
Summary:Drug seeking and drug self-administration in both animals and humans can be triggered by drugs of abuse themselves or by stressful events. Here, we demonstrate that in vivo administration of drugs of abuse with different molecular mechanisms of action as well as acute stress both increase strength at excitatory synapses on midbrain dopamine neurons. Psychoactive drugs with minimal abuse potential do not cause this change. The synaptic effects of stress, but not of cocaine, are blocked by the glucocorticoid receptor antagonist RU486. These results suggest that plasticity at excitatory synapses on dopamine neurons may be a key neural adaptation contributing to addiction and its interactions with stress and thus may be an attractive therapeutic target for reducing the risk of addiction.
ISSN:0896-6273
1097-4199
DOI:10.1016/S0896-6273(03)00021-7