Cabergoline Decreases Alcohol Drinking and Seeking Behaviors Via Glial Cell Line-Derived Neurotrophic Factor

Carnicella, Sébastien; Ahmadiantehrani, Somayeh; He, Dao-Yao; Nielsen, Carsten K.; Bartlett, Selena E.; Janak, Patricia H.; Ron, Dorit

doi:10.1016/j.biopsych.2008.12.022

Cited by 38 publications

(66 citation statements)

References 57 publications

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“…Systemic administration of cabergoline significantly reduces operant ethanol self-administration in rats [230]. Moreover, systemic administration of cabergoline reduced both the reacquisition of operant responding for ethanol after a period of extinction and cue-induces ethanolseeking after abstinence (which represents two different models of relapse) [230].…”

Section: Glial Cell Line-derived Neurotrophic Factor (Gdnf)mentioning

confidence: 98%

Turning the Clock Ahead: Potential Preclinical and Clinical Neuropharmacological Targets for Alcohol Dependence

Leggio¹,

Cardone²,

Ferrulli³

et al. 2010

curr pharm des

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Treating alcohol use disorders represents a main goal in public health, but the effect of current medications is modest. Thus, in the last few years, research has been focusing on identifying new neuropharmacological targets for alcohol dependence. This review will summarize recent research, which has identified new targets to treat alcohol dependence. A variety of systems have been investigated, such as the endocannabinoid system, modulators of glutamatergic transmission, corticotropin-releasing factor (CRF), neuropeptide Y (NPY), nociceptin, glial cell line-derived neurotrophic factor (GDNF), acetaldehyde (ACD), substance P and Neurokinin 1 (NK1) receptor, nicotinic acetylcholine receptors (nAchRs), alpha-adrenergic receptor, and many others. Compared to preclinical studies, only a few clinical studies have been conducted so far. Thus, there is a critical need to translate successful preclinical results into human clinical trials. However, since some clinical studies have failed to replicate preclinical findings, future research will have not only to identify more efficacious medications, but also delineate the best match between a particular pharmacotherapy with a specific alcoholic subtype.

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Section: Glial Cell Line-derived Neurotrophic Factor (Gdnf)mentioning

confidence: 98%

Turning the Clock Ahead: Potential Preclinical and Clinical Neuropharmacological Targets for Alcohol Dependence

Leggio¹,

Cardone²,

Ferrulli³

et al. 2010

curr pharm des

View full text Add to dashboard Cite

show abstract

“…To trigger memory retrieval of operant responding for ethanol, the light cue (CS) and two primes of ethanol (0.1 ml of 10% ethanol, spaced by 1 min) were delivered at the beginning of the test session. Then, each press on the active lever resulted in the delivery of 0.1 ml of 10% ethanol during the entire self-administration session (30 min; Carnicella et al, 2009;Peana et al, 2009). …”

Section: Reacquisition Testingmentioning

confidence: 99%

Fluoxetine, Desipramine, and the Dual Antidepressant Milnacipran Reduce Alcohol Self-Administration and/or Relapse in Dependent Rats

O'Brien

Legastelois

Houchi

et al. 2011

Neuropsychopharmacol

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A few clinical studies have shown that dual antidepressants (serotonergic (5-HT) and noradrenergic (NE) transporter inhibitors, SNRIs) may be effective in alcoholism treatment. We studied the effect of the dual antidepressant milnacipran on ethanol operant self-administration in acutely withdrawn ethanol-dependent and in -non-dependent Wistar rats, and used fluoxetine and desipramine to dissect both 5-HT and NE components, respectively, in the effect of milnacipran. Milnacipran was also tested for relapse after protracted abstinence and on ethanol-induced (1.0 g/kg) conditioned place preference in control rats and ethanol-induced locomotor sensitization in DBA/2J female mice. Milnacipran dose dependently (5-40 mg/kg) attenuated the increased ethanol self-administration observed during early withdrawal and was more potent in preventing reinstatement in dependent rats after protracted abstinence as compared with non-dependent rats. Desipramine and fluoxetine (10 mg/kg) blocked ethanol self-administration during early withdrawal, and recovery was delayed in dependent animals, indicating a potent effect. Ethanol self-administration was also reduced 1 day after treatment with desipramine and fluoxetine but not with milnacipran. Finally, milnacipran prevented ethanol-induced place preference in ethanol-naive rats and reduced the magnitude of ethanol-induced sensitization associated with a delayed induction in mice. Desipramine (20 mg/kg) countered sensitization development and reduced its expression at 1 week after treatment; fluoxetine (10 mg/kg) reduced sensitization expression. Thus, 5-HT and NE transmissions during sensitization expression may mediate the effect of milnacipran on sensitization induction. These results support that SNRIs may have a potential use in alcoholism treatment.

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“…This study showed that microinjection of either quinpirole or quinelorane, into the anterior part of the VTA dose-dependently decreased alcohol, but not sucrose, intake in alcoholpreferring rats [142]. In support are the data showing that local administration of cabergoline into the VTA reduced alcohol-seeking behaviour in rats [170]. These data are contradictory to the findings showing that the dopamine D2 receptor antagonist into the anterior VTA did not alter alcohol intake in high-alcohol-preferring rats [142].…”

Section: Preclinical Evidence For the Use Of Dopamine Agonists To Attmentioning

confidence: 61%

“…Moreover, cabergoline, a dopamine D2 receptor agonist, decreased alcohol intake, relapse drinking as well as alcohol-seeking behaviour in rodents [170]. In addition, low doses of bromocriptine produced a significant, dose-dependent shift in decreasing the preference for alcohol while enhancing water consumption [171], indicating that the compound at lower doses preferentially augment autoreceptor function, leading to decreased dopamine turnover with a blunted response to the rewarding effects of alcohol as a result.…”

Section: Preclinical Evidence For the Use Of Dopamine Agonists To Attmentioning

confidence: 97%

Dopamine and Alcohol Dependence: From Bench to Clinic

Jayaram‐Lindström¹,

Ericson²,

Steensland³

et al. 2016

Recent Advances in Drug Addiction Research and Clinical Applications

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Alcohol dependence, a chronic relapsing psychiatric disorder, is a major cause of mortality and morbidity. The role of dopamine in alcohol-induced reward as well in the development of alcohol dependence is reviewed herein. Both preclinical and clinical studies have suggested that alcohol activates the mesolimbic dopamine system (defined as a dopamine projection from the ventral tegmental area (VTA) to the nucleus accumbens (NAc, i.e. ventral striatum)) leading to a euphoric sensation. Alcohol dependence is characterized by a disruption in the reward-related brain areas including fewer dopamine D2 receptors in ventral striatum. Investigations of the underlying dopaminergic mechanisms involved during the development and maintenance of alcohol dependence could identify novel targets. Human and rodent experimental studies show that dopamine receptor antagonists, agonists and partial agonists as well as dopamine stabilizers influencing dopamine transmission, alter alcohol-mediated behaviours and thus may be potential treatment targets for alcohol dependence. Although there exists promising preclinical results, the majority of placebo-controlled randomized clinical trials with traditional dopamine antagonists and agonists have so far have been discouraging. Furthermore, the severe side-effect profiles of many of these compounds may limit their clinical use. Newer dopamine agents, such as partial agonists and dopamine stabilizers, attenuate alcohol-mediated behaviours in rodents as well as humans. Preclinical as well as clinical studies have shown that substances indirectly targeting the mesolimbic dopamine system may be potential targets for attenuation of alcohol reward. Collectively, the data reviewed herein may contribute to further understanding the complex mechanisms involved in development of alcohol dependence and we suggest that the newer dopamine agents as well as indirect modulators of dopamine signalling deserve to be further evaluated for treatment of alcohol dependence.

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Cabergoline Decreases Alcohol Drinking and Seeking Behaviors Via Glial Cell Line-Derived Neurotrophic Factor

Cited by 38 publications

References 57 publications

Turning the Clock Ahead: Potential Preclinical and Clinical Neuropharmacological Targets for Alcohol Dependence

Turning the Clock Ahead: Potential Preclinical and Clinical Neuropharmacological Targets for Alcohol Dependence

Fluoxetine, Desipramine, and the Dual Antidepressant Milnacipran Reduce Alcohol Self-Administration and/or Relapse in Dependent Rats

Dopamine and Alcohol Dependence: From Bench to Clinic

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