Persistent escalation of alcohol consumption by mice exposed to brief episodes of social defeat stress: suppression by CRF-R1 antagonism

Newman, Emily L.; Albrechet‐Souza, Lucas; Andrew, Peter M.; Auld, John G.; Burk, Kelly; Hwa, Lara S.; Zhang, Eric Y.; DeBold, Joseph F.; Miczek, Klaus A.

doi:10.1007/s00213-018-4905-9

Cited by 40 publications

(27 citation statements)

References 97 publications

(147 reference statements)

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“…previously and consequently escalated their alcohol consumption (Hwa et al 2016;Newman et al 2018). Importantly, CRFR1 antagonist treatment was also shown to increase DA release in the nucleus accumbens (NAc) ( Fig.…”

Section: Candidate Mechanisms For Social Stress: Corticosterone and Cmentioning

confidence: 91%

“…Specifically, 24-h access to 20% w/v ethanol in one of two concurrently available bottles every other day led to persistently and preferentially increased consumption of alcohol (Hwa et al 2011). In a further series of experiments, the interactive effects of two stress manipulations was investigated by initially exposing B6 mice to ten intermittent episodes of social defeat stress and subsequently providing access to alcohol on alternating days in a 2-bottle choice protocol for four weeks (Hwa et al 2016;Newman et al 2018). Both a history of intermittent social defeat stress and intermittent access to alcohol resulted in significant escalation of alcohol consumption relative to non-stressed mice with continuous access to 2-bottle choice of water and alcohol.…”

Section: Intermittent Vs Continuous Access To Alcoholmentioning

confidence: 99%

“…This can also reduce stress-escalated alcohol consumption during continuous or intermittent access (Newman et al 2018).…”

Section: Candidate Mechanisms For Social Stress: Corticosterone and Cmentioning

confidence: 99%

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Non-pharmacological factors that determine drug use and addiction

Ahmed

Badiani

Miczek

et al. 2020

Neuroscience & Biobehavioral Reviews

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Based on their pharmacological properties, psychoactive drugs are supposed to take control of the natural reward system to finally drive compulsory drug seeking and consumption. However, psychoactive drugs are not used in an arbitrary way as pure pharmacological reinforcement would suggest, but rather in a highly specific manner depending on non-pharmacological factors. While pharmacological effects of psychoactive drugs are well studied, neurobiological mechanisms of non-pharmacological factors are less well understood. Here we review the emerging neurobiological mechanisms beyond pharmacological reinforcement which determine drug effects and use frequency. Important progress was made on the understanding of how the character of an environment and social stress determine drug self-administration. This is expanded by new evidence on how behavioral alternatives and opportunities for drug instrumentalization generate different patterns of drug choice. Emerging evidence suggests that the neurobiology of non-pharmacological factors strongly determines pharmacological and behavioral drug action and may, thus, give rise for an expanded system's approach of psychoactive drug use and addiction.

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Section: Candidate Mechanisms For Social Stress: Corticosterone and Cmentioning

confidence: 91%

Section: Intermittent Vs Continuous Access To Alcoholmentioning

confidence: 99%

See 1 more Smart Citation

Non-pharmacological factors that determine drug use and addiction

Ahmed

Badiani

Miczek

et al. 2020

Neuroscience & Biobehavioral Reviews

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“…Ten consecutive days of intermittent social defeat stress can produce significant, persistent increases in voluntary alcohol consumption in both C57BL/6J ( Fig. 1 ; Albrechet-Souza et al, 2017 ; Hwa et al, 2016a ; Newman et al, 2018 ) and outbred, Swiss-derived mice ( Norman et al, 2015 ). During intermittent resident-intruder confrontations, an aggressive, physical encounter is terminated after a fixed duration or number of attack bites (e.g., 5 min or 30 bites).…”

Section: Animal Models Of Social Stress and Pathological Patterns Of mentioning

confidence: 99%

Social defeat stress and escalation of cocaine and alcohol consumption: Focus on CRF

Newman

Leonard

Arena

et al. 2018

Neurobiology of Stress

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Both the ostensibly aversive effects of unpredictable episodes of social stress and the intensely rewarding effects of drugs of abuse activate the mesocorticolimbic dopamine systems. Significant neuroadaptations in interacting stress and reward neurocircuitry may underlie the striking connection between stress and substance use disorders. In rodent models, recurring intermittent exposure to social defeat stress appears to produce a distinct profile of neuroadaptations that translates most readily to the repercussions of social stress in humans. In the present review, preclinical rodent models of social defeat stress and subsequent alcohol, cocaine or opioid consumption are discussed with regard to: (1) the temporal pattern of social defeat stress, (2) male and female protocols of social stress-escalated drug consumption, and (3) the neuroplastic effects of social stress, which may contribute to escalated drug-taking. Neuroadaptations in corticotropin-releasing factor (CRF) and CRF modulation of monoamines in the ventral tegmental area and the bed nucleus of the stria terminalis are highlighted as potential mechanisms underlying stress-escalated drug consumption. However, the specific mechanisms that drive CRF-mediated increases in dopamine require additional investigation as do the stress-induced neuroadaptations that may contribute to the development of compulsive patterns of drug-taking.

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“…We have previously found that exposure to chronic alcohol gavage increases sensitivity to SDS (Nelson et al, ). This relationship is bidirectional, as exposure to chronic SDS can impact drinking behaviors, including consumption (Croft et al, ; Dong et al, ; Hwa et al, ; Karlsson et al, ; Nelson et al, ; Newman et al, ; Newman et al, ; Newman et al, ; Norman et al, ), conditioned place preference (Macedo et al, ), self‐administration (Caldwell and Riccio, ; Rodriguez‐Arias et al, ), and motivation to seek alcohol (Rodriguez‐Arias et al, ). While we have examined the effect of experimenter‐delivered chronic alcohol on sensitivity to SDS, it is important to determine if voluntary alcohol consumption could have a similar effect in mice.…”

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confidence: 99%

Intermittent Ethanol Access Increases Sensitivity to Social Defeat Stress

Nennig

Fulenwider

Eskew

et al. 2020

Alcoholism Clin & Exp Res

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Background Comorbidity between alcoholism and depression is extremely common. Recent evidence supports a relationship between alcohol exposure and stress sensitivity, an underlying factor in the development of depression. Our laboratory has recently shown that chronic alcohol gavage increases sensitivity to social defeat stress (SDS). However, the effects of voluntary alcohol consumption, resulting from protocols such as intermittent ethanol access (IEA), on defeat stress sensitivity have yet to be elucidated. Methods We first assessed the effects of 4 weeks of IEA to 20% alcohol on sensitivity to subthreshold SDS exposure. Next, to examine neuroinflammatory mechanisms, we analyzed gene expression of inhibitor of NFkB (IkB) following IEA or chronic alcohol exposure (10 days of 3.0 g/kg alcohol via intragastric gavage). Then, we quantified NFkB activation via β‐galactosidase immunohistochemistry following IEA or chronic alcohol gavage in NFkB‐LacZ mice. Results IEA‐exposed mice displayed an increase in sensitivity to subthreshold SDS compared to water‐drinking controls. We also found that IkB gene expression was decreased in the nucleus accumbens (NAC) and amygdala (AMY) following IEA but was not altered following chronic alcohol gavage. Finally, we observed increased NFkB activity in the central amygdala (CEA), basolateral amygdala (BLA), and medial amygdala (MEA) after IEA, and increased NFkB activity solely in the CEA following chronic alcohol gavage. Conclusions These findings further corroborate that prior alcohol exposure, in this case intermittent voluntary consumption, can impact development of depressive‐like behavior by altering stress sensitivity. Furthermore, our results suggest the CEA as a potential mediator of alcohol's effects on stress sensitivity, as NFkB was activated in this region following both IEA and chronic alcohol gavage. Thus, this study provides novel insight on alterations in the NFkB pathway and identifies specific regions to target in future experiments assessing the functional role of NFkB in these processes.

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Persistent escalation of alcohol consumption by mice exposed to brief episodes of social defeat stress: suppression by CRF-R1 antagonism

Cited by 40 publications

References 97 publications

Non-pharmacological factors that determine drug use and addiction

Non-pharmacological factors that determine drug use and addiction

Social defeat stress and escalation of cocaine and alcohol consumption: Focus on CRF

Intermittent Ethanol Access Increases Sensitivity to Social Defeat Stress

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