Basolateral amygdala corticotropin-releasing factor receptor type 1 regulates context-cocaine memory strength during reconsolidation in a sex-dependent manner

Ritchie, Jobe L.; Walters, Jennifer L.; Galliou, Justine M; Christian, Robert J.; Qi, Shuyi; Savenkova, Marina I.; Ibarra, Christopher K.; Grogan, Shayna R.; Fuchs, Rita A.

doi:10.1016/j.neuropharm.2021.108819

Cited by 11 publications

(14 citation statements)

References 107 publications

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“…The basolateral amygdala (BLA), a subregion of the amygdala, is closely implicated in learning, memory, and emotional behavior ( Davis, 1992 ; Maren, 2003 ; See et al, 2003 ). Substantial evidence indicates that the BLA is a critical brain region involved in the reconsolidation of drug-related associative memories ( Hellemans et al, 2006 ; Wells et al, 2013 ; Jian et al, 2014 ; Higginbotham et al, 2021 ; Ritchie et al, 2021 ). Two important aspects of memory reconsolidation have been pointed out.…”

Section: Introductionmentioning

confidence: 99%

DNA methyltransferase activity in the basolateral amygdala is critical for reconsolidation of a heroin reward memory

Qian

Shi²,

Huang³

et al. 2022

Front. Mol. Neurosci.

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The persistence of drug memory contributes to relapse to drug seeking. The association between repeated drug exposure and drug-related cues leads to cravings triggered by drug-paired cues. The erasure of drug memories has been considered a promising way to inhibit cravings and prevent relapse. The re-exposure to drug-related cues destabilizes well-consolidated drug memories, during which a de novo protein synthesis-dependent process termed “reconsolidation” occurs to restabilize the reactivated drug memory. Disrupting reconsolidation of drug memories leads to the attenuation of drug-seeking behavior in both animal models and people with addictions. Additionally, epigenetic mechanisms regulated by DNA methyltransferase (DNMT) are involved in the reconsolidation of fear and cocaine reward memory. In the present study, we investigated the role of DNMT in the reconsolidation of heroin reward memory. In the heroin self-administration model in rats, we tested the effects of DNMT inhibition during the reconsolidation process on cue-induced reinstatement, heroin-priming-induced reinstatement, and spontaneous recovery of heroin-seeking behavior. We found that the bilateral infusion of 5-azacytidine (5-AZA) inhibiting DNMT into the basolateral amygdala (BLA) immediately after heroin reward memory retrieval, but not delayed 6 h after retrieval or without retrieval, decreased subsequent cue-induced and heroin-priming-induced reinstatement of heroin-seeking behavior. These findings demonstrate that inhibiting the activity of DNMT in BLA during the reconsolidation of heroin reward memory attenuates heroin-seeking behavior, which may provide a potential strategy for the therapeutic of heroin addiction.

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Section: Introductionmentioning

confidence: 99%

DNA methyltransferase activity in the basolateral amygdala is critical for reconsolidation of a heroin reward memory

Qian

Shi²,

Huang³

et al. 2022

Front. Mol. Neurosci.

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“…Group assignment was balanced based on mean active-lever responding on the last three cocaine self-administration days. The 15-minute session length is sufficient to destabilize cocaine memories without eliciting overt behavioral extinction [11,21]. The rats were connected to the infusion lines, but lever responses were not reinforced.…”

Section: Methodsmentioning

confidence: 99%

“…Standard protocols were used to fluorescently label targets in free-floating brain slices ( [21,25]; see Supplement for details). Briefly, brain slices were placed in blocking solution for 1 hour then incubated with an appropriate primary antibody for 20 or 72 h at 4°C (for CRF protein) or overnight at room temperature (for IEGs and cell-type markers) (antibody information is provided in Table S1).…”

Section: Immunohistochemistrymentioning

confidence: 99%

“…DR neuronal populations can release several neurotransmitters, including glutamate, serotonin, dopamine, and CRF, that have been implicated in memory reconsolidation [16][17][18][19] and alter their firing rate upon the presentation of reward-predictive stimuli [20]. We have demonstrated that DR engagement is critical for cocaine-Corresponding Author: Dr. Rita A. Fuchs, Washington State University, Integrative Physiology and Neuroscience, Veterinary and Biomedical Research Building 205, PO Box 647620, Pullman, WA 99164-7620, Email: rita.fuchs@wsu.edu memory reconsolidation, as GABA agonist-induced inhibition of DR neuronal signaling after memory reactivation weakens cocaine memories and diminishes subsequent context-induced cocaine-seeking behavior [21]. However, the role of DR projections, and specifically DR CRF inputs to the BLA (DRCRF→BLA), in cocaine-memory reconsolidation is not known.…”

Section: Introductionmentioning

confidence: 99%

“…Upstream from these signaling events, corticotropin releasing factor ( CRF ) signaling in the BLA is necessary and sufficient for cocaine-memory reconsolidation. In support of this, intra-BLA CRF receptor type 1 ( CRFR1 ) antagonist administration attenuates cocaine-memory strength, independent of sex, and exogenous CRF administration enhances memory strength in female rats [16]. However, the critical source of BLA CRF during cocaine-memory reconsolidation has not been investigated.…”

Section: Introductionmentioning

confidence: 99%

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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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Corticotropin releasing factor and drug seeking in substance use disorders: Preclinical evidence and translational limitations

Mantsch¹

2022

Addiction Neuroscience

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Basolateral amygdala corticotropin-releasing factor receptor type 1 regulates context-cocaine memory strength during reconsolidation in a sex-dependent manner

Cited by 11 publications

References 107 publications

DNA methyltransferase activity in the basolateral amygdala is critical for reconsolidation of a heroin reward memory

DNA methyltransferase activity in the basolateral amygdala is critical for reconsolidation of a heroin reward memory

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

Corticotropin releasing factor and drug seeking in substance use disorders: Preclinical evidence and translational limitations

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