Abstract
Addiction to cocaine produces long-lasting, stable changes in brain synaptic physiology that might contribute to the vulnerability to relapse. In humans, exposure to environmental contexts previously paired with drug use precipitates relapse, but the neurobiological mechanisms mediating this process are unknown. Initiation of cocaine relapse via re-exposure to a drug-associated context elicited reinstatement of cocaine seeking as well as rapid, transient synaptic plasticity in the nucleus accumbens core (NAcore), measured as an increase in dendritic spine diameter. These results show that rapid context-evoked synaptic potentiation in the NAcore may underpin relapse to cocaine use.
Original language | English |
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Pages (from-to) | 972-974 |
Number of pages | 3 |
Journal | Addiction Biology |
Volume | 19 |
Issue number | 6 |
DOIs | |
State | Published - Nov 1 2014 |
Bibliographical note
Publisher Copyright:© 2013 Society for the Study of Addiction.
Funding
Funders | Funder number |
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National Institutes of Health (NIH) | DA03906, DA012513, DA015369, DA033690 |
National Institute on Drug Abuse | P50DA015369 |
Keywords
- Cocaine
- context-induced relapse
- dendritic spines
- nucleus accumbens core
- synaptic potentiation
ASJC Scopus subject areas
- Medicine (miscellaneous)
- Pharmacology
- Psychiatry and Mental health