Key determinants for morphine withdrawal conditioned context-induced increase in Arc expression in anterior cingulate cortex and withdrawal memory retrieval

Chen, Ming; Shao, Da; Fu, Yali; Ma, Qianqian; Cui, Dongyang; Song, Jiaojiao; Sheng, Huan; Yang, Li; Dong, Yi; Lai, Bin; Zheng, Ping

doi:10.1016/j.expneurol.2018.10.009

Cited by 13 publications

(19 citation statements)

References 48 publications

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“…To study the influence of morphine reward memory reconsolidation on the activity of the IC, we examined the expression of c-Fos, a molecular marker of neuronal activation (Curran and Morgan, 1995;Chen et al, 2019), following retrieval of morphine-cue memory (i.e., CS + US) in the IC using Western blotting (Figures 2A, B). We could see that the expression of c-Fos in the IC significantly increased in the retrieval group (F (2, 14) = 29.28, p < 0 .001, one-way ANOVA followed by Tukey's multiple comparison test, Figures 2C, D).…”

Section: Experiments 1: Drug-cue Memory Retrieval Activates the Icmentioning

confidence: 99%

Postretrieval Microinjection of Baclofen Into the Agranular Insular Cortex Inhibits Morphine-Induced CPP by Disrupting Reconsolidation

Sun

Chang

et al. 2020

Front. Pharmacol.

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Environmental cues associated with drug abuse are powerful mediators of drug craving and relapse in substance-abuse disorders. Consequently, attenuating the strength of cuedrug memories could reduce the number of factors that cause drug craving and relapse. Interestingly, impairing cue-drug memory reconsolidation is a generally accepted strategy aimed at reducing the intensity of cues that trigger drug-seeking and drug-taking behaviors. In addition, the agranular insular cortex (AI) is an important component of the neural circuits underlying drug-related memory reconsolidation. GABA B receptors (GABA B Rs) are potential targets for the treatment of addiction, and baclofen (BLF) is the only prototypical GABA B agonist available for application in clinical addiction treatment. Furthermore, DFosB is considered a biomarker for the evaluation of potential therapeutic interventions for addiction. Here, we used the morphine-induced conditioned place preference (CPP) paradigm to investigate whether postretrieval microinjections of BLF into the AI could affect reconsolidation of drug-reward memory, reinstatement of CPP, and the level of DFosB in mice. Our results showed that BLF infused into the AI immediately following morphine CPP memory retrieval, but not 6 h postretrieval or following nonretrieval, could eliminate the expression of a morphine CPP memory. This effect persisted in a morphine-priming-induced reinstatement test, suggesting that BLF in the AI was capable of preventing the reconsolidation of the morphine CPP memory. Our results also showed that the elimination of morphine CPP memory was associated with reduced morphine-associated DFosB expression in the longer term. Taken together, the results of our research provide evidence to support that GABA B Rs in the AI have an important role in drug-cue memory reconsolidation and further our understanding of the role of the AI in drug-related learning and memory.

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Section: Experiments 1: Drug-cue Memory Retrieval Activates the Icmentioning

confidence: 99%

Postretrieval Microinjection of Baclofen Into the Agranular Insular Cortex Inhibits Morphine-Induced CPP by Disrupting Reconsolidation

Sun

Chang

et al. 2020

Front. Pharmacol.

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“…Conditioned place aversion was conducted with a three-compartment place conditioning apparatus (Med Associates, United States) with distinct visual and tactile environments to maximize contextual differences. The procedure for CPA was similar to that described previously ( Chen et al, 2019 ). On day 1, the pre-conditioning phase (pre-test), the animals were placed in the central neutral area of the apparatus for 2 min to further habituation and then allowed to freely explore all three compartments for 15 min.…”

Section: Methodsmentioning

confidence: 99%

“…On day 11, 24 h after the last conditioning session, animals were re-exposed to the CPA compartments and were allowed to freely explore the entire apparatus for 15 min. CPA score was defined as difference between the time spent in the saline-paired compartment and the time spent in the naloxone-paired compartment (the time in the naloxone-paired compartment minus the time in the saline-paired compartment) ( Wang et al, 2017 ; Chen et al, 2019 ).…”

Section: Methodsmentioning

confidence: 99%

A Conditioning-Strengthened Circuit From CA1 of Dorsal Hippocampus to Basolateral Amygdala Participates in Morphine-Withdrawal Memory Retrieval

Cao

et al. 2020

Front. Neurosci.

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Conditioned context-induced retrieval of drug withdrawal memory contributes to drug relapse. The basolateral amygdala (BLA) is an important brain region that is involved in conditioned context-induced retrieval of morphine withdrawal memory. However, the upstream pathways of the activation of the BLA by conditioned context remains to be studied. The present results show that the CA1 of dorsal hippocampus is an upstream brain region of the activation of the BLA during conditioned context-induced morphine withdrawal memory retrieval; the indirect connection from the CA1 of dorsal hippocampus to the BLA is enhanced in mice with conditioned place aversion (CPA); the postrhinal cortex (POR) is a brain region that connects the CA1 of dorsal hippocampus and the activation of the BLA during conditioned context-induced retrieval of morphine-withdrawal memory. These results suggest that a conditioning-strengthened indirect circuit from the CA1 of dorsal hippocampus to the BLA through the POR participates in morphine withdrawal memory retrieval.

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“…Dendritic spine analysis were performed as previously described (Ming et al, 2018). Briefly, mice were deeply anaesthetized and transcardially perfused.…”

Section: Methodsmentioning

confidence: 99%

Up-Regulation of αCaMKII Impairs Cued Fear Extinction and NMDAR-Dependent LTD in the Lateral Amygdala

Wang

Zhang

et al. 2020

Preprint

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Impaired fear extinction is one of the hallmark symptoms of post-traumatic stress disorder (PTSD). The roles of αCaMKII have been not extensively studied in fear extinction and LTD. Here, we found PTSD susceptible mice exhibited significant up-regulation of αCaMKII in the lateral amygdala (LA). Consistently, increasing αCaMKII in LA profoundly not only caused PTSD-like symptoms such as impaired fear extinction and anxiety-like behaviors, but also attenuated NMDAR-dependent LTD at thalamo-LA synapses, reduced GluA1-Ser845/Ser831 dephosphorylation and AMPAR internalization. Suppressing the elevated αCaMKII to normal level could completely reverse both PTSD-like symptoms and the impairments in LTD, GluA1-Ser845/Ser831 dephosphorylation and AMPAR internalization. Intriguingly, deficits in AMPAR internalization and GluA1-Ser845/Ser831 dephosphorylation were detected not only after impaired fear extinction, but also after attenuated LTD Our results demonstrate for the first time GluA1-Ser845/Ser831 dephosphorylation and AMPAR internalization are molecular links between LTD and fear extinction, and suggest αCaMKII may be a potential molecular determinant of PTSD.

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Key determinants for morphine withdrawal conditioned context-induced increase in Arc expression in anterior cingulate cortex and withdrawal memory retrieval

Cited by 13 publications

References 48 publications

Postretrieval Microinjection of Baclofen Into the Agranular Insular Cortex Inhibits Morphine-Induced CPP by Disrupting Reconsolidation

Postretrieval Microinjection of Baclofen Into the Agranular Insular Cortex Inhibits Morphine-Induced CPP by Disrupting Reconsolidation

A Conditioning-Strengthened Circuit From CA1 of Dorsal Hippocampus to Basolateral Amygdala Participates in Morphine-Withdrawal Memory Retrieval

Up-Regulation of αCaMKII Impairs Cued Fear Extinction and NMDAR-Dependent LTD in the Lateral Amygdala

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