Evidence that vasopressin V1b receptors mediate the transition to excessive drinking in ethanol‐dependent rats

@article{Edwards2012EvidenceTV,
  title={Evidence that vasopressin V1b receptors mediate the transition to excessive drinking in ethanol‐dependent rats},
  author={Scott Edwards and Miguel Guerrero and Ola M Ghoneim and Edward Roberts and George F. Koob},
  journal={Addiction Biology},
  year={2012},
  volume={17}
}
Alcoholism is a devastating condition that represents a progression from initial alcohol use to dependence. Although most individuals are capable of consuming alcohol in a limited fashion, the development of alcohol dependence in a subset of individuals is often associated with negative emotional states (including anxiety and depression). Since the alleviation of this negative motivational state via excessive alcohol consumption often becomes a central goal of alcoholics, the transition from… Expand
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References

SHOWING 1-10 OF 78 REFERENCES
A key role for corticotropin-releasing factor in alcohol dependence
TLDR
The CRF system is emerging as a key element of the neuroadaptive changes driving alcoholism and as a major target for its treatment. Expand
Corticotropin-Releasing Factor 1 Antagonists Selectively Reduce Ethanol Self-Administration in Ethanol-Dependent Rats
TLDR
These data demonstrate that CRF(1) receptors play an important role in mediating excessive ethanol self-administration in dependent rats, with no effect in nondependent rats, and may be exciting new pharmacotherapeutic targets for the treatment of alcoholism in humans. Expand
Chronic ethanol ingestion modulates proanxiety factors expressed in rat central amygdala.
TLDR
These findings suggest that adaptations to chronic ethanol exposure by proanxiety factors expressed in the central nucleus appear to be mediated by distinct cellular and molecular mechanisms. Expand
Neurobiology of Alcohol Dependence: Focus on Motivational Mechanisms
TLDR
Recent research focusing on brain arousal, reward, and stress systems is accelerating the understanding of the components of alcohol dependence and contributing to the development of new treatment strategies. Expand
The role of arginine vasopressin in alcohol tolerance.
TLDR
Mechanisms by which vasopressin can produce long-term changes in central nervous system function are suggested, and evidence for a disturbance of vasopressingin regulation during chronic ethanol ingestion is provided. Expand
Decreased brain reward produced by ethanol withdrawal.
TLDR
The results suggest that decreased function of reward systems (elevations in reward thresholds) is a common element of withdrawal from chronic administration of several diverse classes of abused drugs. Expand
Excessive Ethanol Drinking Following a History of Dependence: Animal Model of Allostasis
TLDR
Results indicate that operant responding for ethanol was enhanced during protracted abstinence by 30–100% and remained elevated for 4–8 weeks post acute withdrawal, which has important implications for understanding the characteristics and mechanisms underlying vulnerability to relapse. Expand
Pharmacological Evidence for a Motivational Role of κ-Opioid Systems in Ethanol Dependence
The purpose of this study was to test the hypothesis that activation of the dynorphin/kappa (κ)-opioid system has a role in the increased consumption of ethanol in dependent animals. The effects ofExpand
Upregulation of Voluntary Alcohol Intake, Behavioral Sensitivity to Stress, and Amygdala Crhr1 Expression Following a History of Dependence
TLDR
Alcohol drinking was upregulated long-term following a history of dependence and fear suppression of behavior was selectively potentiated in postdependent animals. Expand
Arginine vasopressin maintains ethanol tolerance
TLDR
Evidence is presented that treatment of animals with AVP during and after chronic ethanol administration leads to long-term maintenance of tolerance to the hypothermic and sedative effects of ethanol. Expand
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