Social defeat stress selectively alters mesocorticolimbic dopamine release: an in vivo microdialysis study

Tidey, Jennifer W.; Miczek, Klaus A.

doi:10.1016/0006-8993(96)00159-x

Cited by 456 publications

(343 citation statements)

References 35 publications

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“…We postulate that elevations in the functional activity of CeA cells are a direct result of the stress-induced deficit in mPFC activation. Episodic stress-induced increases of DA and glutamate in the mPFC (Perez-Jaranay and Vives, 1991; Tidey and Miczek, 1996) may represent the substrate underlying the observed social stress-induced deficit of mPFC functional activity. The mPFC directly inhibits the activity of amygdala neurons, and cortical inhibition of the CeA overrides other inputs to the CeA, including that from the BLA (Rosenkranz and Grace, 2001;Quirk et al, 2003).…”

Section: Discussionmentioning

confidence: 99%

“…Social defeat is a salient stressor characterized by a distinctive physiological profile and cellular activation of mesocorticolimbic pathways (Miczek et al, 1982;Tidey and Miczek, 1996;Kollack-Walker et al, 1997;Martinez et al, 2002;Miczek et al, 2004). The amygdala and medial prefrontal cortex (mPFC) are essential for initiating appropriate behavioral and physiological responses to stressful challenges, and one of their functions is to maintain control over conditioned reinforced behavior (Doherty and Gratton, 1996;Jentsch and Taylor, 1999;Parkinson et al, 2000;Stevenson and Gratton, 2003).…”

Section: Introductionmentioning

confidence: 99%

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Brief Social Defeat Stress: Long Lasting Effects on Cocaine Taking During a Binge and Zif268 mRNA Expression in the Amygdala and Prefrontal Cortex

Covington

Kikusui

Goodhue

et al. 2004

Neuropsychopharmacol

112

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Social stress can engender behavioral and neural sensitization and this process appears to enhance the transition to compulsive drug abuse. Exposures to brief social defeat stress in rats have significant consequences on cocaine-reinforced behavior and on the level of functional activation within regions of the mesocorticolimbic dopamine system. The objectives of the current study were to examine the enduring consequences of brief episodes of social defeat stress on cocaine bingeing (during 24 h of continuous access) and on the emergence of neural adaptations as revealed by zif268 immediate early gene expression. Adult, male Long-Evans rats were subjected to four 25 min episodes of social defeat (once every 72 h). After 2 months, cocaine binges or zif268 mRNA gene expression were studied after confirming behavioral cross-sensitization to stimulant challenge. Sensitization to social defeat increased cocaine intake during a 24 h binge, effectively abolishing the typical circadian pattern of intake. Furthermore, 60 days after exposure to the sensitizing regimen of social defeat, levels of functional activation, measured by zif268 mRNA expression, in the central and medial amygdala were increased, while levels of activation in the medial prefrontal cortex were decreased. Persistent stress-induced levels of zif268 in the central and medial amygdala were attenuated by an injection of amphetamine (1.0 mg/kg). Divergent changes in zif268 within the amygdala and cortex 2 months after social defeat stress indicate the vulnerability of distinct cellular populations in networks that modulate the behavioral actions of psychomotor stimulants.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Brief Social Defeat Stress: Long Lasting Effects on Cocaine Taking During a Binge and Zif268 mRNA Expression in the Amygdala and Prefrontal Cortex

Covington

Kikusui

Goodhue

et al. 2004

Neuropsychopharmacol

112

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“…Taken together, only animals that experienced defeat in a social interaction with a dominant resident displayed a reinstatement of ethanol-induced CPP, suggesting that chronic social stress is as effective as physical stress in reinstating drug seeking. At the molecular level, it has been reported that the mesocorticolimbic dopamine system was activated following social defeat stress (Burke et al 2013;Tidey and Miczek 1996;Wand et al 2007;Yavich and Tiihonen 2000), and therefore this system could be involved in chronic social stress-induced reinstatement of ethanol seeking behavior. In addition, Nikulina and co-workers have reported that within 30 min after social defeat stress in rats, the expression levels of μ-opioid receptor (MOR)-encoding mRNA, as evaluated and quantified by in situ hybridization, increased in the lateral ventral tegmental area (VTA) (Nikulina et al 1999).…”

Section: Consequences Of Csc On Body Weight Gain and Anxiety-like Behmentioning

confidence: 99%

Chronic psychosocial stress causes delayed extinction and exacerbates reinstatement of ethanol-induced conditioned place preference in mice

Bahí

Dreyer

2013

Psychopharmacology

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Rationale We have shown previously, using an animal model of voluntary ethanol intake and ethanol-conditioned place preference (EtOH-CPP), that exposure to chronic psychosocial stress induces increased ethanol intake and EtOH-CPP acquisition in mice. Objective Here, we examined the impact of chronic subordinate colony (CSC) exposure on EtOH-CPP extinction, as well as ethanol-induced reinstatement of CPP. Methods Mice were conditioned with saline or 1.5 g/kg ethanol and were tested in the EtOH-CPP model. In the first experiment, the mice were subjected to 19 days of chronic stress, and EtOH-CPP extinction was assessed during seven daily trials without ethanol injection. In the second experiment and after the EtOH-CPP test, the mice were subjected to 7 days of extinction trials before the 19 days of chronic stress. Druginduced EtOH-CPP reinstatement was induced by a priming injection of 0.5 g/kg ethanol. Results Compared to the single-housed colony mice, CSC mice exhibited increased anxiety-like behavior in the elevated plus maze (EPM) and the open field tests. Interestingly, the CSC mice showed delayed EtOH-CPP extinction. More importantly, CSC mice showed increased alcohol-induced reinstatement of the EtOH-CPP behavior. Conclusion Taken together, this study indicates that chronic psychosocial stress can have long-term effects on EtOH-CPP extinction as well as drug-induced reinstatement behavior and may provide a suitable model to study the latent effects of chronic psychosocial stress on extinction and relapse to drug abuse.

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“…Importantly, however, a role for DA has not been ruled out. For example, acute stress rapidly activates DA neurons in the VTA [144] and increases DA release in the NAc [143,260,289] and mPFC [277,312]. Stress-induced elevation of NAc DA correlates temporally with reinstatement of heroin seeking [259].…”

Section: Summary Of Effects Of Sb-277011-a On Addictive Drug Actionmentioning

confidence: 99%

The role of central dopamine D3 receptors in drug addiction: a review of pharmacological evidence

Heidbreder

Gardner

et al. 2005

Brain Research Reviews

305

249

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The cDNA for the dopamine D 3 receptor was isolated and characterized in 1990. Subsequent studies have indicated that D 3 receptors, as well as D 3 receptor mRNA, are primarily localized in limbic regions in mammals. This finding led to the postulate that D 3 receptors may be involved in drug dependence and addiction. However, this hypothesis has been difficult to test due to the lack of compounds with high selectivity for central D 3 receptors. The interpretation of results from studies using mixed D 2 /D 3 agonists and/or antagonists is problematic because these agents have low selectivity for D 3 over D 2 receptors and it is likely that their actions are primarily related to D 2 receptor antagonism and possibly interaction with other neurotransmitter receptors. Currently, with the synthesis and characterization of new highly selective D 3 receptor antagonists such as SB-277011-A this difficulty has been surmounted. The purpose of the present article is to review, for the first time, the effects of various putative D 3 receptor selective compounds in animal models of drug dependence and addiction. The results obtained with highly selective D 3 receptor antagonists such as SB-277011-A, SB-414796, and NGB-2904 indicate that central D 3 receptors may play an important role in drug-induced reward, drug-taking, and cue-, drug-, and stressinduced reinstatement of drug-seeking behavior. Provided these results can be extrapolated to human drug addicts, they suggest that selective DA D 3 receptor antagonists may prove effective as potential pharmacotherapeutic agents to manage drug dependence and addiction.

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Social defeat stress selectively alters mesocorticolimbic dopamine release: an in vivo microdialysis study

Cited by 456 publications

References 35 publications

Brief Social Defeat Stress: Long Lasting Effects on Cocaine Taking During a Binge and Zif268 mRNA Expression in the Amygdala and Prefrontal Cortex

Brief Social Defeat Stress: Long Lasting Effects on Cocaine Taking During a Binge and Zif268 mRNA Expression in the Amygdala and Prefrontal Cortex

Chronic psychosocial stress causes delayed extinction and exacerbates reinstatement of ethanol-induced conditioned place preference in mice

The role of central dopamine D3 receptors in drug addiction: a review of pharmacological evidence

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