Modulating reconsolidation and extinction to regulate drug reward memory.

Modulating reconsolidation and extinction to regulate drug reward memory.
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DOI:
10.1111/ejn.14072
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发表时间:
2019-08
期刊:
The European journal of neuroscience
影响因子:
--
通讯作者:
Li JX
Li JX
中科院分区:
其他
文献类型:
--
作者:
Liu JF;Tian J;Li JX

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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 memoires. 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 and non-pharmacological modulation of reconsolidation and extinction are promising approaches to regulate drug reward memory and prevent relapse. Interventions targeting drug reward memory are promising strategies for addiction treatment. After exposure to drug-associated cues, drug reward memory can enter two opposing processes: reconsolidation and extinction. Here, we review the pharmacological and behavioral modulations on the reconsolidation and extinction of drug reward memory.
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