Role of prefrontal cortex in the extinction of drug memories

Zhang, Wenhua; Cao, Kexin; Ding, Zhixia; Yang, Jianli; Pan, Bing‐Xing; Xue, Yan-Xue

doi:10.1007/s00213-018-5069-3

Cited by 18 publications

(7 citation statements)

References 172 publications

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“…Both make the case that the neural circuitry supporting fear memory extinction and drug memory extinction overlaps markedly; with both being dependent on the communication between subcortical regions, such as the amygdala, and prefrontal cortical regions. The requirement for prefrontal cortex in appetitive memory extinction is further underscored in an in-depth review from Xue and colleagues (Zhang et al 2019). Pertinently, a report from Müller Ewald et al (2019) shows, using an optogenetic approach, that the contribution of the (infralimbic) prefrontal cortex to the reduction of cocaine-seeking depends upon the subjects’ prior extinction training.…”

Section: The Psychopharmacology Of Reward and Drug Extinctionmentioning

confidence: 99%

Editorial: the psychopharmacology of extinction—from theory to therapy

Milton

Holmes

2019

Psychopharmacology

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Section: The Psychopharmacology Of Reward and Drug Extinctionmentioning

confidence: 99%

Editorial: the psychopharmacology of extinction—from theory to therapy

Milton

Holmes

2019

Psychopharmacology

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“…It receives robust glutamatergic inputs from multiple limbic regions [e.g., basolateral amygdala (BLA) and ventral hippocampus] and from the medial and lateral prefrontal cortex (PFCx) ( Groenewegen et al, 1999 ; Ikemoto, 2007 ). While the PFCx is responsible for planning, evaluating long-term consequences and is instrumental in retrieving drug-associated memories ( Dalley et al, 2004 ; Zhang et al, 2019 ), the BLA encodes emotions that shape impulsive behavior and the response to associative learning ( Gallagher and Chiba, 1996 ; Cardinal et al, 2002 ; Lalumiere, 2014 ). Importantly, PFCx and BLA send converging synaptic inputs onto single GABAergic medium-spiny neurons (MSNs) ( O’Donnell and Grace, 1995 ; Finch, 1996 ; French and Totterdell, 2002 ), the only output cells of the NAc that represent up to 95% of the NAc neuronal population ( Meredith and Totterdell, 1999 ).…”

Section: Introductionmentioning

confidence: 99%

Binge Alcohol Drinking Alters Synaptic Processing of Executive and Emotional Information in Core Nucleus Accumbens Medium Spiny Neurons

Kolpakova

Vinne

Giménez-Gómez

et al. 2021

Front. Cell. Neurosci.

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The nucleus accumbens (NAc) is a forebrain region mediating the positive-reinforcing properties of drugs of abuse, including alcohol. It receives glutamatergic projections from multiple forebrain and limbic regions such as the prefrontal cortex (PFCx) and basolateral amygdala (BLA), respectively. However, it is unknown how NAc medium spiny neurons (MSNs) integrate PFCx and BLA inputs, and how this integration is affected by alcohol exposure. Because progress has been hampered by the inability to independently stimulate different pathways, we implemented a dual wavelength optogenetic approach to selectively and independently stimulate PFCx and BLA NAc inputs within the same brain slice. This approach functionally demonstrates that PFCx and BLA inputs synapse onto the same MSNs where they reciprocally inhibit each other pre-synaptically in a strict time-dependent manner. In alcohol-naïve mice, this temporal gating of BLA-inputs by PFCx afferents is stronger than the reverse, revealing that MSNs prioritize high-order executive processes information from the PFCx. Importantly, binge alcohol drinking alters this reciprocal inhibition by unilaterally strengthening BLA inhibition of PFCx inputs. In line with this observation, we demonstrate that in vivo optogenetic stimulation of the BLA, but not PFCx, blocks binge alcohol drinking escalation in mice. Overall, our results identify NAc MSNs as a key integrator of executive and emotional information and show that this integration is dysregulated during binge alcohol drinking.

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“…Recent studies focused on understanding the circuitry and cellular mechanisms underlying extinction of drug-associated behavior have provided compelling evidence for the involvement of glutamatergic, dopaminergic, and noradrenergic plasticity in the nucleus accumbens (NAc), amygdala (Amy), and prefrontal cortex (PFC) (Torregrossa et al, 2010;Gass and Chandler, 2013;Goode and Maren, 2019;Zhang et al, 2019). Some of the extinction-related neuroplastic changes involve brain-derived neurotropic factor (BDNF) and AMPA receptor (GlueA1 and GluA2) (Xue et al, 2014), both of which are deemed for their critical roles in long-term memory and drug addiction (Cleva et al, 2010;Barker et al, 2015).…”

Section: Introductionmentioning

confidence: 99%

Berberine Facilitates Extinction of Drug-Associated Behavior and Inhibits Reinstatement of Drug Seeking

et al. 2020

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A high rate of relapse is a major clinical problem among drug-addicted individuals. Persistent traces of drug-associated reward memories contribute to intense craving and often trigger relapse. A number of interventions on drug-associated memories have shown significant benefits in relapse prevention. Among them are pre-or post-extinction pharmacological manipulations that facilitate the extinction of drug-associated behavior. Berberine, a bioactive isoquinoline alkaloid, has been recently reported to provide therapeutic benefits for a number of central nervous system (CNS) disorders, including morphine addiction. The present study aimed to investigate whether berberine could serve as a post-extinction pharmacological intervention agent to reduce risks of reinstatement of drug seeking. We found that an intragastric administration of berberine at doses of 25 and 50 mg/kg during the critical time window significantly facilitated the extinction of morphine-reward related behavior in free access and confined conditioned place preference (CPP) extinction paradigms, and subsequently, it prevented reinstatement and spontaneous recovery of morphine-induced CPP in mice. Intriguingly, the berberine treatment with or without extinction training altered expression of plasticity-related proteins such as brain-derived neurotrophic factor (BDNF), AMPA receptors (GluA1 and GluA2) in the nucleus accumbens (NAc). Moreover, the post-extinction berberine treatment significantly reduced reinstatement of cocaine-induced CPP and operant intravenous self-administration (IVSA) memories in rats. Altogether, our findings suggest that extinction training combined with the postextinction berberine treatment can facilitate extinction of drug-associated behavior making it an attractive therapeutic candidate in relapse prevention.

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Role of prefrontal cortex in the extinction of drug memories

Cited by 18 publications

References 172 publications

Editorial: the psychopharmacology of extinction—from theory to therapy

Editorial: the psychopharmacology of extinction—from theory to therapy

Binge Alcohol Drinking Alters Synaptic Processing of Executive and Emotional Information in Core Nucleus Accumbens Medium Spiny Neurons

Berberine Facilitates Extinction of Drug-Associated Behavior and Inhibits Reinstatement of Drug Seeking

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