Bidirectional modulation of incubation of cocaine craving by silent synapse-based remodeling of prefrontal cortex to accumbens projections
2014-09-17 | journal article; research paper
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Bidirectional modulation of incubation of cocaine craving by silent synapse-based remodeling of prefrontal cortex to accumbens projections
Ma, Y.-Y.; Lee, B. R.; Wang, X.; Guo, C.; Liu, L.; Cui, R. & Lan, Y. et al. (2014)
Neuron, 83(6) pp. 1453-1467. DOI: https://doi.org/10.1016/j.neuron.2014.08.023
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Details
- Authors
- Ma, Yao-Ying; Lee, Brian R.; Wang, Xiusong; Guo, Changyong; Liu, Lei; Cui, Ranji; Lan, Yan; Balcita-Pedicino, Judith J.; Wolf, Marina E.; Sesack, Susan R.; Shaham, Yavin; Schlüter, Oliver M. ; Huang, Yanhua H.; Dong, Yan
- Abstract
- Glutamatergic projections from the medial prefrontal cortex (mPFC) to nucleus accumbens (NAc) contribute to cocaine relapse. Here we show that silent synapse-based remodeling of the two major mPFC-to-NAc projections differentially regulated the progressive increase in cue-induced cocaine seeking after withdrawal (incubation of cocaine craving). Specifically, cocaine self-administration in rats generated AMPA receptor-silent glutamatergic synapses within both infralimbic (IL) and prelimbic mPFC (PrL) to NAc projections, measured after 1 day of withdrawal. After 45 days of withdrawal, IL-to-NAc silent synapses became unsilenced/matured by recruiting calcium-permeable (CP) AMPARs, whereas PrL-to-NAc silent synapses matured by recruiting non-CP-AMPARs, resulting in differential remodeling of these projections. Optogenetic reversal of silent synapse-based remodeling of IL-to-NAc and PrL-to-NAc projections potentiated and inhibited, respectively, incubation of cocaine craving on withdrawal day 45. Thus, pro- and antirelapse circuitry remodeling is induced in parallel after cocaine self-administration. These results may provide substrates for utilizing endogenous antirelapse mechanisms to reduce cocaine relapse.
- Issue Date
- 17-September-2014
- Journal
- Neuron
- ISSN
- 0896-6273
- eISSN
- 1097-4199
- Language
- English