The role of corticotrophin-releasing factor in stress-induced relapse to alcohol-seeking behavior in rats

Lê, A. D.; Harding, Stephen E.; Juzytsch, Walter; Watchus, Jason; Shalev, Uri; Shaham, Yavin

doi:10.1007/s002130000411

Cited by 287 publications

(117 citation statements)

References 56 publications

Supporting

Mentioning

107

Contrasting

Unclassified

Order By: Relevance

“…However, the role of other mediators of the stress response was not excluded, and pharmacological activation of the kappa system by drug injection may also affect the HPA (Iyengar et al, 1986). Corticosterone has been implicated elsewhere as a mediator in stress-induced increases in drug self-administration (Piazza et al, 1990;Deroche-Gamonet et al, 2003;Shalev et al, 2003), although other studies have suggested this hormone is either not involved (Shaham et al, 1997;Lê et al, 2000) or only indirectly involved (Erb et al, 1998). Our results showed that treatments that blocked swim stress-induced potentiation of cocaine-CPP (ie nor-BNI pretreatment, KOR gene deletion, prodynorphin gene deletion) did not block swim stressinduced increases in serum corticosterone levels.…”

Section: Discussioncontrasting

confidence: 52%

Prior Activation of Kappa Opioid Receptors by U50,488 Mimics Repeated Forced Swim Stress to Potentiate Cocaine Place Preference Conditioning

McLaughlin

Land

et al. 2005

Neuropsychopharmacol

201

240

View full text Add to dashboard Cite

Repeated forced-swim stress (FSS) produced analgesia, immobility and potentiation of cocaine-conditioned place preference (CPP) in wild-type C57Bl/6 mice, but not in littermates lacking the kappa opioid receptor (KOR) gene. These results were surprising because kappa agonists are known to produce conditioned place aversion and to suppress cocaine-CPP when coadministered with cocaine. The possibility that disruption of the kappa system blocked the stress response by adversely affecting the hypothalamic-pituitary axis was examined by measuring plasma corticosterone levels. However, disruption of the dynorphin/kappa system by gene deletion or receptor antagonism did not reduce the FSS-induced elevation of plasma corticosterone levels. A second explanation for the difference is that kappa receptor activation caused by FSS occurred prior to cocaine conditioning rather than contemporaneously. To test this hypothesis, we measured the effects of the kappa agonist (trans)-3,4-dichloro-N-methyl-N-[2-(1-pyrrolidinyl)-cyclohexyl]benzeneacetamide (U50,488) administered to mice at various intervals preceding cocaine conditioning. The results showed that the interaction between the kappa system and cocaine reinforcement depended on the timing of the drug pairing. Mice given U50,488 60 min prior to cocaine showed a robust, nor-BNI-sensitive potentiation of cocaine-CPP, whereas administration 15 min before cocaine significantly suppressed cocaine-CPP. In the absence of cocaine, U50,488 given 60 min prior to saline conditioning produced no place preference, whereas administration 15 min before saline conditioning produced significant place aversion. The results of this study suggest that kappa receptor activation induced by FSS prior to the cocaine-conditioning session may be both necessary and sufficient for potentiation of the reinforcing actions of cocaine.

show abstract

Section: Discussioncontrasting

confidence: 52%

Prior Activation of Kappa Opioid Receptors by U50,488 Mimics Repeated Forced Swim Stress to Potentiate Cocaine Place Preference Conditioning

McLaughlin

Land

et al. 2005

Neuropsychopharmacol

201

240

View full text Add to dashboard Cite

show abstract

“…Reinstatement of drug seeking is also obtained with administration of the α-2 adrenoreceptor antagonist yohimbine, which, by increasing brain noradrenaline cell firing (Aghajanian and VanderMaelen 1982) and release (Abercrombie et al 1988), acts as a pharmacological stressor (Bremner et al 1996a,b;Charney et al 1983;Holmberg et al 1962;Lee et al 2004;Lê et al 2000Lê et al , 2005. These two methods were used to investigate the effect of URB597 on stress-induced alcohol seeking.…”

Section: Reinstatement Testingmentioning

confidence: 99%

Increase of brain endocannabinoid anandamide levels by FAAH inhibition and alcohol abuse behaviours in the rat

et al. 2008

View full text Add to dashboard Cite

Rationale A major clinical concern with the use of cannabinoid receptor 1 (CB1) direct agonists is that these compounds increase alcohol drinking and drug abuserelated behaviours. As an alternative approach, CB1-receptor-mediated activity can be facilitated by increasing anandamide levels with the use of hydrolase fatty acid amide hydrolase (FAAH) inhibitors. Objective Using the selective FAAH inhibitor URB597, we investigated whether activation of the endogenous cannabinoid tone increases alcohol abuse liability, as what happens with the CB1 receptor direct agonists.Materials and methods URB597 was tested on alcohol self-administration in Wistar rats and on homecage alcohol drinking in genetically selected Marchigian Sardinian alcohol-preferring (msP) rats. In Wistar rats, URB597 effects on alcohol-induced anxiety and on stress-, yohimbineand cue-induced reinstatement of alcohol seeking were also evaluated. For comparison, the effect of the CB1 receptor antagonist rimonabant on ethanol self-administration was also tested. Results Under our experimental condition, intraperitoneal (IP) administration of URB597 (0.0, 0.3 and 1.0 mg/kg) neither increased voluntary homecage alcohol drinking in msP rats nor facilitated fixed ratio 1 and progressive ratio alcohol self-administration in nonselected Wistars. In the reinstatement tests, the compound did not have effects on cue-, footshock stress-and yohimbine-induced relapse. Conversely, URB597 completely abolished the anxiogenic response measured during withdrawal after an acute IP administration of alcohol (3.0 g/kg). Rimonabant (0.0, 0.3, 1.0 and 3.0 mg/kg) significantly reduced ethanol self-administration. Conclusions Results demonstrate that activation of the endocannabinoid anandamide system by selective inhibition of FAAH does not increase alcohol abuse risks but does reduce anxiety associated to alcohol withdrawal. We thus can speculate that medication based on the use of endocannabinoid system modulators such as URB597 may offer important advantages compared to treatment with direct CB1 receptor activators.

show abstract

“…3). The ability of stress to increase alcohol seeking (Lê et al 1998(Lê et al , 1999(Lê et al , 2000Weiss 2002a, 2003;Martin-Fardon et al 2000) is consistent with stress enhancing the probability of relapse and furthering alcohol abuse. Further, the risk of relapse in alcoholics is reportedly increased by stress (Brown et al 1990(Brown et al , 1995Pohorecky 1991;Sinha 2001), with anxiety during abstinence being a predictor of endstate drinking (Kushner et al 1994(Kushner et al , 2000(Kushner et al , 2001Sloan et al 2003;Willinger et al 2002).…”

Section: Stress During Withdrawal From Multiple Alcohol Exposures Incmentioning

confidence: 76%

“…Likewise, stress can increase alcohol-seeking behavior (Lê et al 1998(Lê et al , 1999(Lê et al , 2000Weiss 2002b, 2003;Martin-Fardon et al 2000;Weiss et al 2001). In fact, stress is a more powerful stimulus for alcohol seeking than "priming" doses of alcohol (Lê et al 1998).…”

Section: Stress During Withdrawal From Multiple Alcohol Exposures Incmentioning

confidence: 99%

Conceptual framework for the etiology of alcoholism: a ?kindling?/stress hypothesis

2004

View full text Add to dashboard Cite

Rationale-The rationale for proposing the "kindling"/stress hypothesis is to provide a conceptual basis for the insidious development and maintenance of alcohol abuse.Objective and results-An objective of the hypothesis is to emphasize how continued alcohol abuse is linked to progressive neural adaptation. Work has shown that repeated withdrawals from chronic low levels of alcohol sensitize ("kindle") anxiety-like behavior ("anxiety") in rats, a finding consistent with multiple withdrawal kindling of seizure activity. Additionally, stress substitutes for initial cycles of the multiple withdrawal protocol to sensitize withdrawal-induced anxiety, which is indicative that stress is capable of facilitating neuroadaptive processes related to withdrawal. The persistence of adaptation caused by stress and multiple withdrawals is revealed by the appearance of withdrawal-induced anxiety following a future re-exposure to a single 5-day period of alcohol. This persisting adaptation also permits stress to induce anxiety during a period of abstinence-a response not observed in animals without previous exposure to alcohol. Furthermore, stress interacts with repeated withdrawals to enhance voluntary alcohol drinking. Results of other preclinical and clinical studies reported in the literature are integrated with these investigations in support of the proposed hypothesis.Conclusions-The "kindling"/stress hypothesis is based on the premise that repeated withdrawals from cycles of chronic alcohol exposure contribute to a progressive development of persisting adaptive change that sensitizes withdrawal-induced anxiety and allows stress to evoke symptoms associated with negative affect during abstinence. Thus, these consequences of repeated withdrawals account for the evolution of major characteristics of alcoholism, which include worsened acute withdrawal symptoms and increased stress-induced negative affect during abstinence, both of which enhance the likelihood of relapse-and with relapse an inability to limit an abusive pattern of alcohol intake. The "kindling"/stress hypothesis provides a clear strategy for future studies to explore the advancing neural adaptation proposed to contribute to the pathogenesis of alcoholism.

show abstract

The role of corticotrophin-releasing factor in stress-induced relapse to alcohol-seeking behavior in rats

Abstract: These data suggest that CRF contributes to stress-induced relapse to alcohol seeking via its actions on extra-hypothalamic sites. The present data, and previous data with heroin- and cocaine-trained rats, point to a general role of CRF in relapse to drugs induced by stressors.

Cited by 287 publications

References 56 publications

Prior Activation of Kappa Opioid Receptors by U50,488 Mimics Repeated Forced Swim Stress to Potentiate Cocaine Place Preference Conditioning

Prior Activation of Kappa Opioid Receptors by U50,488 Mimics Repeated Forced Swim Stress to Potentiate Cocaine Place Preference Conditioning

Increase of brain endocannabinoid anandamide levels by FAAH inhibition and alcohol abuse behaviours in the rat

Conceptual framework for the etiology of alcoholism: a ?kindling?/stress hypothesis

Contact Info

Product

Resources

About