Modulating reconsolidation and extinction to regulate drug reward memory
- PMID: 30113098
- PMCID: PMC6377866
- DOI: 10.1111/ejn.14072
Modulating reconsolidation and extinction to regulate drug reward memory
Abstract
Drug addiction is an aberrant memory that shares the same memory processes as other memories. Brief exposure to drug-associated cues could result in reconsolidation, a hypothetical process during which original memory could be updated. In contrast, longer exposure times to drug-associated cues could trigger extinction, a process that decreases the conditioned responding. In this review, we discuss the pharmacological and non-pharmacological manipulations on the reconsolidation and extinction that could be used to interfere with drug reward memories. Pharmacological agents such as β-adrenergic receptor antagonist propranolol can interfere with reconsolidation to disrupt drug reward memory. Pharmacological agents such as the NMDA receptor glycine site agonists d-cycloserine and d-serine can facilitate extinction and then attenuate the expression of drug reward memory. Besides pharmacological interventions, drug-free behavioral approaches by utilizing the reconsolidation and extinction, such as 'post-retrieval extinction' and 'UCS-retrieval extinction', are also effective to erase or inhibit the recall of drug reward memory. Taken together, pharmacological modulation and non-pharmacological modulation of reconsolidation and extinction are promising approaches to regulate drug reward memory and prevent relapse.
Keywords: drug addiction; drug reward memory; extinction; reconsolidation; relapse.
© 2018 Federation of European Neuroscience Societies and John Wiley & Sons Ltd.
Conflict of interest statement
Conflict of interest
The authors declare no conflict of interest.
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