Isolation and striatal (3H) serotonin uptake: Role in the voluntary intake of ethanol by rats

Daoust, M.; Chrétien, Pierre; Moore, N; Saligaut, Christian; Lhuintre, J. P.; Boismare, F

doi:10.1016/0091-3057(85)90378-8

Cited by 40 publications

(12 citation statements)

References 17 publications

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“…In addition, a polymorphism in the promoter region of the human and nonhuman primate 5-HTT gene, which confers low-expression of 5-HTT, has been associated with alcoholism and certain neuropsychiatric disorders that are frequently comorbid with the disease, such as anxiety and depression (Thompson et al, 2000;Kranzler et al, 2002;Barr et al, 2004a,b). Together, these findings support a possible role for the 5-HTT in modulating the effects of ethanol on brain 5-HT and, further, suggest that the level of 5-HTT function or expression may impact the behavioral effects of ethanol (Roach et al, 1973;Daoust et al, 1985Daoust et al, , 1991aLe Marquand et al, 1994).…”

Section: Introductionmentioning

confidence: 75%

Ethanol Inhibits Clearance of Brain Serotonin by a Serotonin Transporter-Independent Mechanism

Daws

Montañez

Munn

et al. 2006

Journal of Neuroscience

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Section: Introductionmentioning

confidence: 75%

Ethanol Inhibits Clearance of Brain Serotonin by a Serotonin Transporter-Independent Mechanism

Daws

Montañez

Munn

et al. 2006

Journal of Neuroscience

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“…Both preference and operant ethanol-reinforced behavior paradigms have been used to study the effects of 5-HT re-uptake inhibition on ethanol drinking in animal models. Inhibition of 5-HT re-uptake has usually been shown to decrease voluntary consumption of ethanol solutions using the preference paradigm (Geller 1973;Daoust et al 1985;Zabik et al 1985;Gill et al 1988aGill et al , 1988b. While these animal studies have shown that treatment with serotonin reuptake inhibitors (SSRIs) can suppress ethanol consumption, there has been debate as to whether suppression of ethanol intake is due to reductions in its reinforcing effects, or the result of generalized decreases in consummatory behavior (Blundell and Latham 1982;Blundell 1984).…”

Section: Serotoninmentioning

confidence: 97%

Neuropharmacological treatments for alcoholism: scientific basis and clinical findings

Johnson¹,

Ait-Daoud

2000

Psychopharmacology

159

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Preclinical studies have exploded our knowledge about the behavioral and biological underpinnings of alcoholism. These studies suggest that certain neurotransmitters, particularly those interacting with the opioid, N-methyl-D-aspartate, and monoamine systems, may play a critical role in the expression of alcohol-drinking and other behaviors associated with its abuse liability. Built upon this foundation, important advances have been made in the development of therapeutic medications for the treatment of alcoholism. Of the medications reviewed, acamprosate's potential appears to be the most widely established. In the USA, naltrexone was approved by the Food and Drug Administration in 1995 for the treatment of alcoholism; however, the results of some studies have been less encouraging. Naltrexone's reliance on high compliance rates for efficacy may, eventually, limit its potential in clinical settings offering generic treatment for alcoholism. The relative paucity of dose-response studies on naltrexone's effects in treating alcoholics is an important gap in the literature. Recent data from a large clinical trial suggests that ondansetron, a serotonin3 antagonist, offers new hope for the treatment of early onset alcoholics; a type of alcoholism most difficult to manage with psychosocial measures alone. Different subtypes of alcoholic may, therefore, have varying treatment responses to serotonergic agents. Matching subtypes of alcoholic to effective treatment medications based upon their different biologies remains an important therapeutic goal. Combinations of effective pharmacological agents need exploration as they may prove to be synergistic, and could shepherd in a new era of treatments aimed at multiple neurotransmitter targets associated with the alcoholism disease. The coming decade promises more powerful tools for characterizing drug effects on alcohol drinking, thereby closing the gap between animal models of addiction and the human condition.

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“…While a majority of reports on isolation in rats confirm the increased alcohol consumption following isolation described above [30–37], decades of literature examining effects of isolation on alcohol intake include some apparent contradictions; some studies report no difference in voluntary alcohol intake in response to isolation stress, while few even report a decrease. As suggested by Schenk et al , there are a number of procedural differences that make direct comparisons between studies difficult.…”

Section: Effects Of Housing Conditions On Alcohol Intakementioning

confidence: 99%

Biological Contribution to Social Influences on Alcohol Drinking: Evidence from Animal Models

Anacker¹,

Ryabinin²

2010

IJERPH

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Social factors have a tremendous influence on instances of heavy drinking and in turn impact public health. However, it is extremely difficult to assess whether this influence is only a cultural phenomenon or has biological underpinnings. Research in non-human primates demonstrates that the way individuals are brought up during early development affects their future predisposition for heavy drinking, and research in rats demonstrates that social isolation, crowding or low social ranking can lead to increased alcohol intake, while social defeat can decrease drinking. Neurotransmitter mechanisms contributing to these effects (i.e., serotonin, GABA, dopamine) have begun to be elucidated. However, these studies do not exclude the possibility that social effects on drinking occur through generalized stress responses to negative social environments. Alcohol intake can also be elevated in positive social situations, for example, in rats following an interaction with an intoxicated peer. Recent studies have also begun to adapt a new rodent species, the prairie vole, to study the role of social environment in alcohol drinking. Prairie voles demonstrate a high degree of social affiliation between individuals, and many of the neurochemical mechanisms involved in regulation of these social behaviors (for example, dopamine, central vasopressin and the corticotropin releasing factor system) are also known to be involved in regulation of alcohol intake. Naltrexone, an opioid receptor antagonist approved as a pharmacotherapy for alcoholic patients, has recently been shown to decrease both partner preference and alcohol preference in voles. These findings strongly suggest that mechanisms by which social factors influence drinking have biological roots, and can be studied using rapidly developing new animal models.

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Isolation and striatal (3H) serotonin uptake: Role in the voluntary intake of ethanol by rats

Cited by 40 publications

References 17 publications

Ethanol Inhibits Clearance of Brain Serotonin by a Serotonin Transporter-Independent Mechanism

Ethanol Inhibits Clearance of Brain Serotonin by a Serotonin Transporter-Independent Mechanism

Neuropharmacological treatments for alcoholism: scientific basis and clinical findings

Biological Contribution to Social Influences on Alcohol Drinking: Evidence from Animal Models

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