Heroin relapse requires long-term potentiation-like plasticity mediated by NMDA2b-containing receptors
Persistent relapse to addictive drugs constitutes the most challenging problem in addiction therapy, and is linked to impaired prefrontal cortex regulation of motivated behaviors involving the nucleus accumbens. Using a rat model of heroin addiction, we show that relapse requires long-term potentiat...
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| Published in | Proceedings of the National Academy of Sciences - PNAS Vol. 108; no. 48; pp. 19407 - 19412 |
|---|---|
| Main Authors | , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
National Academy of Sciences
29.11.2011
National Acad Sciences |
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| Online Access | Get full text |
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| Abstract | Persistent relapse to addictive drugs constitutes the most challenging problem in addiction therapy, and is linked to impaired prefrontal cortex regulation of motivated behaviors involving the nucleus accumbens. Using a rat model of heroin addiction, we show that relapse requires long-term potentiation (LTP)-like increases in synaptic strength in the prefrontal cortex projection to the nucleus accumbens. The increased synaptic strength was paralleled by dendritic spine enlargement in accumbens spiny neurons and required up-regulated surface expression of NMDA2b-containing receptors (NR2B). Accordingly, blocking NR2B before reinstating heroin-seeking prevented the induction of LTP-like changes in spine remodeling and synaptic strength, and inhibited heroin relapse. These data show that LTP-like neuroplasticity in prefrontal-accumbens synapses is initiated by NR2B stimulation and strongly contributes to heroin relapse. Moreover, the data reveal NR2B-containing NMDA receptors as a previously unexplored therapeutic target for treating heroin addiction. |
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| AbstractList | Persistent relapse to addictive drugs constitutes the most challenging problem in addiction therapy, and is linked to impaired prefrontal cortex regulation of motivated behaviors involving the nucleus accumbens. Using a rat model of heroin addiction, we show that relapse requires long-term potentiation (LTP)-like increases in synaptic strength in the prefrontal cortex projection to the nucleus accumbens. The increased synaptic strength was paralleled by dendritic spine enlargement in accumbens spiny neurons and required up-regulated surface expression of NMDA2b-containing receptors (NR2B). Accordingly, blocking NR2B before reinstating heroin-seeking prevented the induction of LTP-like changes in spine remodeling and synaptic strength, and inhibited heroin relapse. These data show that LTP-like neuroplasticity in prefrontal-accumbens synapses is initiated by NR2B stimulation and strongly contributes to heroin relapse. Moreover, the data reveal NR2B-containing NMDA receptors as a previously unexplored therapeutic target for treating heroin addiction. [PUBLICATION ABSTRACT] Persistent relapse to addictive drugs constitutes the most challenging problem in addiction therapy, and is linked to impaired prefrontal cortex regulation of motivated behaviors involving the nucleus accumbens. Using a rat model of heroin addiction, we show that relapse requires long-term potentiation (LTP)-like increases in synaptic strength in the prefrontal cortex projection to the nucleus accumbens. The increased synaptic strength was paralleled by dendritic spine enlargement in accumbens spiny neurons and required up-regulated surface expression of NMDA2b-containing receptors (NR2B). Accordingly, blocking NR2B before reinstating heroin-seeking prevented the induction of LTP-like changes in spine remodeling and synaptic strength, and inhibited heroin relapse. These data show that LTP-like neuroplasticity in prefrontal-accumbens synapses is initiated by NR2B stimulation and strongly contributes to heroin relapse. Moreover, the data reveal NR2B-containing NMDA receptors as a previously unexplored therapeutic target for treating heroin addiction. |
| Author | Moussawi, Khaled Toda, Shigenobu Shen, Haowei Zhou, Wenhua Kalivas, Peter W |
| Author_xml | – sequence: 1 fullname: Shen, Haowei – sequence: 2 fullname: Moussawi, Khaled – sequence: 3 fullname: Zhou, Wenhua – sequence: 4 fullname: Toda, Shigenobu – sequence: 5 fullname: Kalivas, Peter W |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/22084102$$D View this record in MEDLINE/PubMed |
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| Notes | Author contributions: H.S. and P.W.K. designed research; H.S., K.M., W.Z., and S.T. performed research; H.S., K.M., W.Z., S.T., and P.W.K. analyzed data; and H.S. and P.W.K. wrote the paper. Edited by Leslie Lars Iversen, University of Oxford, Oxford, United Kingdom, and approved October 17, 2011 (received for review July 28, 2011) |
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| Snippet | Persistent relapse to addictive drugs constitutes the most challenging problem in addiction therapy, and is linked to impaired prefrontal cortex regulation of... |
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| SubjectTerms | Amino acids Analysis of Variance animal models Animals Behavioral neuroscience Biological Sciences Biotinylation Cocaine cortex Dendrites - ultrastructure Dendritic spines drugs Electrophysiology Extinction, Psychological - physiology Gene expression Heroin Heroin Dependence - physiopathology Long-Term Potentiation - physiology Microscopy, Confocal N methyl D aspartate receptors Neurochemistry Neurons Nucleus accumbens Piperidines Prefrontal Cortex - physiology Rats Rats, Sprague-Dawley receptors Receptors, N-Methyl-D-Aspartate - metabolism Recurrence Relapse Rodents Self Administration Small interfering RNA Synapses Synaptic Transmission - physiology therapeutics |
| Title | Heroin relapse requires long-term potentiation-like plasticity mediated by NMDA2b-containing receptors |
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