Cortical and amygdalar neuronal ensembles in alcohol seeking, drinking and withdrawal

George, Olivier; Hope, Bruce T.

doi:10.1016/j.neuropharm.2017.04.031

Cited by 35 publications

(20 citation statements)

References 88 publications

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“…Instead our findings should be integrated with previous work in which dichotomies were observed, along with other studies involving, e.g., response inhibition, to identify how different behavioral tasks differentially engage mPFC subregions. We also note that a focus on neuronal ensembles and networks should be emphasized in future work (Gabbott et al, 2005; Bossert et al, 2011; Moorman et al, 2015; Pfarr et al, 2015; Warren et al, 2016; George and Hope, 2017; Kim et al, 2017). It is possible that different findings across studies may result from differentially targeting subregional circuits (e.g., mPFC projections to NAc core, shell, or amygdala).…”

Section: Discussionmentioning

confidence: 99%

Differential Effects of Dorsal and Ventral Medial Prefrontal Cortex Inactivation during Natural Reward Seeking, Extinction, and Cue-Induced Reinstatement

Caballero¹,

Scarpa

Remage‐Healey

et al. 2019

eNeuro

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Rodent dorsal medial prefrontal cortex (mPFC), typically prelimbic cortex, is often described as promoting actions such as reward seeking, whereas ventral mPFC, typically infralimbic cortex, is thought to promote response inhibition. However, both dorsal and ventral mPFC are necessary for both expression and suppression of different behaviors, and each region may contribute to different functions depending on the specifics of the behavior tested. To better understand the roles of dorsal and ventral mPFC in motivated behavior we pharmacologically inactivated each area during operant fixed ratio 1 (FR1) seeking for a natural reward (sucrose), extinction, cue-induced reinstatement, and progressive ratio (PR) sucrose seeking in male Long–Evans rats. Bilateral inactivation of dorsal mPFC, but not ventral mPFC increased reward seeking during FR1. Inactivation of both dorsal and ventral mPFC decreased seeking during extinction. Bilateral inactivation of ventral mPFC, but not dorsal mPFC decreased reward seeking during cue-induced reinstatement. No effect of inactivation was found during PR. Our data contrast sharply with observations seen during drug seeking and fear conditioning, indicating that previously established roles of dorsal mPFC = going versus ventral mPFC = stopping are not applicable to all motivated behaviors and/or outcomes. Our results indicate that dichotomous functions of dorsal versus ventral mPFC, if they exist, may align better with other models, or may require the development of a new framework in which these multifaceted brain areas play different roles in action control depending on the behavioral context in which they are engaged.

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Section: Discussionmentioning

confidence: 99%

Differential Effects of Dorsal and Ventral Medial Prefrontal Cortex Inactivation during Natural Reward Seeking, Extinction, and Cue-Induced Reinstatement

Caballero¹,

Scarpa

Remage‐Healey

et al. 2019

eNeuro

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“…For example, George et al (2012) quantified Fos in ROIs within the prefrontal cortex (PFC), amygdala and hippocampus of alcohol dependent rats. Withdrawal from alcohol was associated with a decrease in correlated activity between the mPFC and the CeA suggesting that alcohol use and abstinence may specifically modify this segment of the neural circuit that controls alcohol consumption ( George and Hope, 2017 ). The Fos results in this example provide a reliable foundation and justification for conducting riskier tract-specific mechanistic experiments to test the involvement of the circuit model in vivo.…”

Section: Novel Approaches In Using Fos Signalingmentioning

confidence: 99%

What does the Fos say? Using Fos-based approaches to understand the contribution of stress to substance use disorders

McReynolds

Christianson

Blacktop

et al. 2018

Neurobiology of Stress

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Despite extensive research efforts, drug addiction persists as a largely unmet medical need. Perhaps the biggest challenge for treating addiction is the high rate of recidivism. While many factors can promote relapse in abstinent drug users, the contribution of stress is particularly problematic, as stress is uncontrollable and pervasive in the lives of those struggling with addiction. Thus, understanding the neurocircuitry that underlies the influence of stress on drug seeking is critical for guiding treatment. Preclinical research aimed at defining this neurocircuitry has, in part, relied upon the use of experimental approaches that allow visualization of cellular and circuit activity that corresponds to stressor-induced drug seeking in rodent relapse models. Much of what we have learned about the mechanisms that mediate stressor-induced relapse has been informed by studies that have used the expression of the immediate early gene, cfos, or its protein product, Fos, as post-mortem activity markers. In this review we provide an overview of the rodent models used to study stressor-induced relapse and briefly summarize what is known about the underlying neurocircuitry before describing the use of cfos/Fos-based approaches. In addition to reviewing findings obtained using this approach, its advantages and limitations are considered. Moreover, new techniques that leverage the expression profile of cfos to tag and manipulate cells based on their activity patterns are discussed. The intent of the review is to guide the interpretation of old and design of new studies that utilize cfos/Fos-based strategies to study the neurocircuitry that contributes to stress-related drug use.

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“…A challenge in alcohol research is to explain how specific cues or contexts are paired with states of craving, while explaining which mechanisms of brain encoding are involved in these associations. It is hypothesized that the understanding of how specific neuronal ensembles encode and mediate the recall of learned associations among the cues, contexts, and behaviors during alcohol seeking and drinking will be helpful for the comprehension of how baclofen works in the treatment of AUD ( 17 ).…”

Section: Introductionmentioning

confidence: 99%

A Review of the Potential Mechanisms of Action of Baclofen in Alcohol Use Disorder

Beaurepaire

2018

Front. Psychiatry

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Baclofen, a GABA-B receptor agonist, is a promising treatment for alcohol use disorder (AUD). Its mechanism of action in this condition is unknown. GABA-B receptors interact with many biological systems potentially involved in AUD, including transduction pathways and neurotransmitter systems. Preclinical studies have shown that GABA-B receptors are involved in memory storage and retrieval, reward, motivation, mood and anxiety; neuroimaging studies in humans show that baclofen produces region-specific alterations in cerebral activity; GABA-B receptor activation may have neuroprotective effects; baclofen also has anti-inflammatory properties that may be of interest in the context of addiction. However, none of these biological effects fully explain the mechanism of action of baclofen in AUD. Data from clinical studies have provided a certain number of elements which may be useful for the comprehension of its mechanism of action: baclofen typically induces a state of indifference toward alcohol; the effective dose of baclofen in AUD is extremely variable from one patient to another; higher treatment doses correlate with the severity of the addiction; many of the side effects of baclofen resemble those of alcohol, raising the possibility that baclofen acts as a substitution drug; usually, however, there is no tolerance to the effects of baclofen during long-term AUD treatment. In the present article, the biological effects of baclofen are reviewed in the light of its clinical effects in AUD, assuming that, in many instances, clinical effects can be reliable indicators of underlying biological processes. In conclusion, it is proposed that baclofen may suppress the Pavlovian association between cues and rewards through an action in a critical part of the dopaminergic network (the amygdala), thereby normalizing the functional connectivity in the reward network. It is also proposed that this action of baclofen is made possible by the fact that baclofen and alcohol act on similar brain systems in certain regions of the brain.

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Cortical and amygdalar neuronal ensembles in alcohol seeking, drinking and withdrawal

Cited by 35 publications

References 88 publications

Differential Effects of Dorsal and Ventral Medial Prefrontal Cortex Inactivation during Natural Reward Seeking, Extinction, and Cue-Induced Reinstatement

Differential Effects of Dorsal and Ventral Medial Prefrontal Cortex Inactivation during Natural Reward Seeking, Extinction, and Cue-Induced Reinstatement

What does the Fos say? Using Fos-based approaches to understand the contribution of stress to substance use disorders

A Review of the Potential Mechanisms of Action of Baclofen in Alcohol Use Disorder

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