The effect of a methadone-initiated memory reconsolidation updating procedure in opioid use disorder: A translational study

Yue, Jing-Li; Yuan, Kai; Bao, Yanping; Meng, Shi-Qiu; Shi, Le; Qing, Feng‐Ling; Guo, Xiaojie; Cao, Lu; Sun, Yekun; Lu, Tangsheng; Zeng, Na; Yan, Wei; Han, Ying; Sun, Jun; Shi, Jie; Kosten, Thomas R.; Xue, Yan-Xue; Wu, Ping; Lü, Lin

doi:10.1016/j.ebiom.2022.104283

Cited by 10 publications

(4 citation statements)

References 32 publications

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“…Many human studies have identi ed this phenomenon in individuals with a history of taking nicotine 34 , methamphetamine 35 , alcohol 36 , or cocaine 37 . Emerging evidence support that drug craving stemmed from past experiences about drug use which can be encoded and stored in memory, suggesting that memory serves as the foundation of drug craving 2,10,38,39 . Here, our results further demonstrate homogeneity between the enhancement of remote drug-cue associated memory and the incubation of drug craving.…”

Section: Discussionmentioning

confidence: 99%

“…Thus, we speculate that the stable memory is a prerequisite for persistent drug craving during abstinence, and the enhancement of remote drug-cue memory driven by memory consolidation leads to the increased cue-induced drug craving 40 . Although direct evidence is still scarce, many indirect studies have shown that disrupting the memory reconsolidation process can attenuate cue-induced drug craving 12,39 . Therefore, it is worthy to explore the ways in which the enhancement of drug memories causes an abnormal intensi cation of drug craving.…”

Section: Discussionmentioning

confidence: 99%

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Memory consolidation drives the enhancement of remote cocaine memory via prefrontal circuit

Liu,

Lu,

Chen

et al. 2024

Mol Psychiatry

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Remote memory usually decreases over time, whereas remote drug-cue associated memory exhibits enhancement, increasing the risk of relapse during abstinence. Memory system consolidation is a prerequisite for remote memory formation, but neurobiological underpinnings of the role of consolidation in the enhancement of remote drug memory are unclear. Here, we found that remote cocaine-cue associated memory was enhanced in rats that underwent self-administration training, together with a progressive increase in the response of prelimbic cortex (PrL) CaMK neurons to cues. System consolidation was required for the enhancement of remote cocaine memory through PrL CaMK neurons during the early period post-training. Furthermore, dendritic spine maturation in the PrL relied on the basolateral amygdala (BLA) input during the early period of consolidation, contributing to remote memory enhancement. These ndings indicate that memory consolidation drives the enhancement of remote cocaine memory through a time-dependently increase in activity and maturation of PrL CaMK neurons receiving a sustained BLA input.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Memory consolidation drives the enhancement of remote cocaine memory via prefrontal circuit

Liu,

Lu,

Chen

et al. 2024

Mol Psychiatry

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“…1 ), or use of pharmacological agents with similar neurochemical effects but reduced abuse liability (e.g. methylphenidate for psychostimulants [ 63 ] or methadone for opioids [ 201 ]), would be sufficient to destabilise the instrumental memory underlying drug-seeking remains an important outstanding question.…”

Section: The Reconsolidation Of Instrumental Drug-associated Memoriesmentioning

confidence: 99%

Drug memory reconsolidation: from molecular mechanisms to the clinical context

Milton

2023

Transl Psychiatry

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Since its rediscovery at the beginning of the 21st Century, memory reconsolidation has been proposed to be a therapeutic target for reducing the impact of emotional memories that can go awry in mental health disorders such as drug addiction (substance use disorder, SUD). Addiction can be conceptualised as a disorder of learning and memory, in which both pavlovian and instrumental learning systems become hijacked into supporting drug-seeking and drug-taking behaviours. The past two decades of research have characterised the details of the molecular pathways supporting the reconsolidation of pavlovian cue-drug memories, with more recent work indicating that the reconsolidation of instrumental drug-seeking memories also relies upon similar mechanisms. This narrative review considers what is known about the mechanisms underlying the reconsolidation of pavlovian and instrumental memories associated with drug use, how these approaches have translated to experimental medicine studies, and the challenges and opportunities for the clinical use of reconsolidation-based therapies.

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“…The retrieval of such drug memories can elicit drug craving and relapse in individuals with substance use disorder (SUD), but it can also temporarily destabilize those memories [3]. Labile drug memories must be reconsolidated into long-term memory stores to endure [3], and disruption of labile drug memories or interference with their reconsolidation curtails stimulus control over drug-seeking behavior in animal models of drug relapse [4,5] and drug-cue reactivity in substance users [6][7][8][9]. Thus, therapeutic strategies that target labile drug memories or reconsolidation may be promising for relapse prevention [10], but refinement of such approaches requires deeper understanding of underlying neurobiological mechanisms.…”

Section: Introductionmentioning

confidence: 99%

Dorsal Raphe to Basolateral Amygdala Corticotropin-Releasing Factor Circuit Regulates Cocaine-Memory Reconsolidation

Ritchie,

Qi,

Soto

et al. 2024

Preprint

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Environmental stimuli elicit drug craving and relapse in cocaine users by triggering the retrieval of strong cocaine-related contextual memories. Retrieval can also destabilize drug memories, requiring reconsolidation, a protein synthesis-dependent storage process, to maintain memory strength. Corticotropin-releasing factor (CRF) signaling in the basolateral amygdala (BLA) is necessary for cocaine-memory reconsolidation. We have hypothesized that a critical source of CRF in the BLA is the dorsal raphe nucleus (DR) based on its neurochemistry, anatomical connectivity, and requisite involvement in cocaine-memory reconsolidation. To test this hypothesis, male and female Sprague-Dawley rats received adeno-associated viruses to express Gi-coupled designer receptors exclusively activated by designer drugs (DREADDs) selectively in CRF neurons of the DR and injection cannulae directed at the BLA. The rats were trained to self-administer cocaine in a distinct environmental context then received extinction training in a different context. They were then briefly re-exposed to the cocaine-predictive context to destabilize (reactivate) cocaine memories. Intra-BLA infusions of the DREADD agonist deschloroclozapine (DCZ; 0.1 mM, 0.5 μL/hemisphere) after memory reactivation attenuated cocaine-memory strength, relative to vehicle infusion. This was indicated by a selective, DCZ-induced and memory reactivation-dependent decrease in drug-seeking behavior in the cocaine-predictive context in DREADD-expressing males and females at test compared to respective controls. Notably, BLA-projecting DR CRF neurons that exhibited increased c-Fos expression during memory reconsolidation co-expressed glutamatergic and serotonergic neuronal markers. Together, these findings suggest that the DRCRF→ BLA circuit is engaged to maintain cocaine-memory strength after memory destabilization, and this phenomenon may be mediated by DR CRF, glutamate, and/or serotonin release in the BLA.

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The effect of a methadone-initiated memory reconsolidation updating procedure in opioid use disorder: A translational study

Cited by 10 publications

References 32 publications

Memory consolidation drives the enhancement of remote cocaine memory via prefrontal circuit

Memory consolidation drives the enhancement of remote cocaine memory via prefrontal circuit

Drug memory reconsolidation: from molecular mechanisms to the clinical context

Dorsal Raphe to Basolateral Amygdala Corticotropin-Releasing Factor Circuit Regulates Cocaine-Memory Reconsolidation

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