Prevention and reversal of social stress-escalated cocaine self-administration in mice by intra-VTA CRFR1 antagonism

Han, Xiao; DeBold, Joseph F.; Miczek, Klaus A.

doi:10.1007/s00213-017-4676-8

Cited by 31 publications

(32 citation statements)

References 44 publications

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“…; Hansson et al . ; Han, DeBold, & Miczek ; Leonard, DeBold, & Miczek ). A remaining open question is whether msP and Wistar rats differ also in their propensity to relapse in response to environmental cues.…”

Section: Discussionmentioning

confidence: 99%

phMRI, neurochemical and behavioral responses to psychostimulants distinguishing genetically selected alcohol‐preferring from genetically heterogenous rats

et al. 2018

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Alcoholism is often associated with other forms of drug abuse, suggesting that innate predisposing factors may confer vulnerability to addiction to diverse substances. However, the neurobiological bases of these factors remain unknown. Here, we have used a combination of imaging, neurochemistry and behavioral techniques to investigate responses to the psychostimulant amphetamine in Marchigian Sardinian (msP) alcohol-preferring rats, a model of vulnerability to alcoholism. Specifically, we employed pharmacological magnetic resonance imaging to investigate the neural circuits engaged by amphetamine challenge, and to relate functional reactivity to neurochemical and behavioral responses. Moreover, we studied self-administration of cocaine in the msP rats. We found stronger functional responses in the extended amygdala, alongside with increased release of dopamine in the nucleus accumbens shell and augmented vertical locomotor activity compared with controls. Wistar and msP rats did not differ in operant cocaine selfadministration under short access (2 hours) conditions, but msP rats exhibited a higher propensity to escalate drug intake following long access (6 hours). Our findings suggest that neurobiological and genetic mechanisms that convey vulnerability to excessive alcohol drinking also facilitate the transition from psychostimulants use to abuse.

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Section: Discussionmentioning

confidence: 99%

phMRI, neurochemical and behavioral responses to psychostimulants distinguishing genetically selected alcohol‐preferring from genetically heterogenous rats

et al. 2018

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“…The effects of SD on cocaine SA have been extensively studied in adult rats (Miczek et al., ). Miczek's laboratory has persistently reported that SD increases both acquisition of cocaine SA and motivation to take the drug, raising the breaking point in the progressive ratio program (Boyson et al., ; Covington et al., ; Han et al., ; Quadros & Miczek, ). Studies use short‐term access to the drug, resulting in very controlled and stable levels of drug SA.…”

Section: Effects Of Social Defeat On Psychostimulant and Alcohol Rewardmentioning

confidence: 99%

“…Social stress promotes the release of CRF in the VTA when there is both acute and repeated social stress (Holly et al., ). Recently, researchers have related this increase in basal levels of CRF in the VTA with the escalation on cocaine SA and the development of behavioral and neural cross‐sensitization that takes place in defeated animals (Boyson et al., ; Han et al., ; Holly et al., ). These CRF effects are mediated by two receptors, namely CRF receptor type 1 (CRFR1) and CRF receptor type 2 (CRFR2), both positively coupled to adenylate cyclase through stimulatory G proteins (Binder & Nemeroff, ; Hauger, Risbrough, Oakley, Olivares‐Reyes, & Dautzenberg, ; Zorrilla & Koob, ).…”

Section: Mechanisms Underlying the Effects Of Social Defeat Stress Onmentioning

confidence: 99%

“…Exposure to different procedures of SD increases the reinforcing effects of cocaine, amphetamine and alcohol. Most studies have used the intravenous self‐administration (SA) paradigm (Han, DeBold, & Miczek, ; Holly et al., ; Neisewander, Peartree, & Pentkowski, ); moreover, consistent results have also been obtained in the conditioned place preference (CPP) paradigm (Montagud‐Romero et al., ; Rodriguez‐Arias et al., , ).…”

Section: Introductionmentioning

confidence: 99%

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Social defeat stress: Mechanisms underlying the increase in rewarding effects of drugs of abuse

Montagud‐Romero

Blanco-Gandía

Reguilón

et al. 2018

Eur J of Neuroscience

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Social interaction is known to be the main source of stress in human beings, which explains the translational importance of this research in animals. Evidence reported over the last decade has revealed that, when exposed to social defeat experiences (brief episodes of social confrontations during adolescence and adulthood), the rodent brain undergoes remodeling and functional modifications, which in turn lead to an increase in the rewarding and reinstating effects of different drugs of abuse. The mechanisms by which social stress cause changes in the brain and behavior are unknown, and so the objective of this review is to contemplate how social defeat stress induces long-lasting consequences that modify the reward system. First of all, we will describe the most characteristic results of the short- and long-term consequences of social defeat stress on the rewarding effects of drugs of abuse such as psychostimulants and alcohol. Secondly, and throughout the review, we will carefully assess the neurobiological mechanisms underlying these effects, including changes in the dopaminergic system, corticotrophin releasing factor signaling, epigenetic modifications and the neuroinflammatory response. To conclude, we will consider the advantages and disadvantages and the translational value of the social defeat stress model, and will discuss challenges and future directions.

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“…Acute stress influences a host of behaviors through the actions of CRF in the VTA, with effects on motivation, decision-making, subsequent drug intake, and drug seeking [3,4,6,7,[20][21][22]. Intriguingly, midbrain CRF suppresses dopamine-dependent behaviors in drugnaïve animals [3,4], whereas CRF promotes dopamine-dependent behaviors in drug-experienced animals [6,7,[20][21][22]. These conflicting reports indicate that the behavioral effects of CRF in the midbrain are either reinforcer-specific, or alternatively depend upon prior drug experience.…”

Section: Discussionmentioning

confidence: 99%

Cocaine experience abolishes the motivation suppressing effect of CRF in the ventral midbrain

Oliva

Donate

Lefner

et al. 2019

Preprint

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Stress affects dopamine-dependent behaviors in part through the actions of corticotropin releasing factor (CRF) in the ventral tegmental area (VTA). In particular, CRF signaling in the VTA mediates how acute stress suppresses the motivation to work for food rewards, as well as how stress promotes drug seeking behavior. These diverging behavioral effects in food-and drug-based tasks could indicate that CRF modulates goal-directed actions in a reinforcer-specific manner. Alternatively, prior drug experience could functionally alter how CRF in the VTA regulates dopamine-dependent behavior. To address these possibilities, we examined how intra-VTA injections of CRF influenced cocaine intake and whether prior drug experience alters how CRF modulates the motivation for food rewards. Our results demonstrate that intra-VTA injections of CRF had no effect on drug intake when self-administering cocaine under a progressive ratio reinforcement schedule. We also found that a prior history of either contingent or non-contingent cocaine infusions abolished the capacity for CRF to reduce the motivation for food rewards. Furthermore, voltammetry recordings in the nucleus accumbens illustrate that CRF in the VTA had no effect on cocaine-evoked dopamine release. These results collectively illustrate that exposure to abused substances functionally alters how neuropeptides act within the VTA to influence motivated behavior. Introduction:Stress induces the release of corticotropin releasing factor (CRF), which is responsible for initiating the hormonal and physiological responses to stress [1]. CRF signaling within the mesocorticolimbic system also mediates the effects of stress on motivation and decision-making processes [2]. For example, CRF receptor activation within the ventral tegmental area (VTA) is required for the stress-induced reduction in the motivation to work for food rewards [3]. Acute stress also decreases the preference for high effort / large reward options in decision making tasks [4]. This alteration in effort-based decision making is blocked by antagonizing CRF receptors and recapitulated by administering CRF directly into the VTA [4]. Therefore, the actions of CRF in the ventral midbrain are critical for how stress regulates behavioral responding for natural rewards.Whereas acute stress reduces the motivation to work for food rewards, stress promotes the reinstatement of drug seeking in a CRF-dependent manner [5]. Antagonizing CRF receptors in the VTA prevents stress-induced cocaine seeking [6,7]. Furthermore, intra-VTA injections of CRF are sufficient to reinstate cocaine seeking in the absence of stress [6,7], which together highlights the involvement of midbrain CRF signaling in how stress promotes drug-dependent behaviors.

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Prevention and reversal of social stress-escalated cocaine self-administration in mice by intra-VTA CRFR1 antagonism

Cited by 31 publications

References 44 publications

phMRI, neurochemical and behavioral responses to psychostimulants distinguishing genetically selected alcohol‐preferring from genetically heterogenous rats

phMRI, neurochemical and behavioral responses to psychostimulants distinguishing genetically selected alcohol‐preferring from genetically heterogenous rats

Social defeat stress: Mechanisms underlying the increase in rewarding effects of drugs of abuse

Cocaine experience abolishes the motivation suppressing effect of CRF in the ventral midbrain

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