Role of dopamine in behavioral sensitization to ethanol in DBA/2J mice

Broadbent, Julie; Kampmueller, Kathryn M.; Koonse, Sharon A.

doi:10.1016/j.alcohol.2005.03.006

Cited by 35 publications

(28 citation statements)

References 35 publications

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“…route, an effective method to test acute alcohol actions (Redetzki et al, 1983;Broadbent et al, 2005). The lack of significant increase in the uptake of leptin and albumin within this short time suggests that the adaptive changes of the BBB might require a higher dose or longer duration of exposure.…”

Section: Discussionmentioning

confidence: 99%

Increased Leptin Permeation across the Blood–Brain Barrier after Chronic Alcohol Ingestion

Pan

Barron

Hsuchou

et al. 2007

Neuropsychopharmacol

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Leptin, a polypeptide mainly produced in the periphery, crosses the blood-brain barrier (BBB) by receptor-mediated transport to exert multiple central nervous system actions including decreased food intake. The reciprocal interactions between leptin transport and alcohol drinking are not clear. In this study, we tested whether alcohol increases leptin entry into brain and, if this occurs, whether it is a consequence of a generalized increase in the permeability of the BBB. BBB permeability to albumin, the increased permeation of which indicates BBB disruption, as well as to leptin was measured after alcohol ingestion. CD1 and B6 mice ingested a 5% liquid alcohol diet or its isocaloric control for 2 weeks. Alcohol ingestion resulted in increased blood-alcohol levels, decreased blood-leptin concentrations, and increased permeation of radioactively labeled leptin across the BBB as shown by in situ perfusion. Although the increased influx of the vascular marker albumin into brain showed partial disruption of the BBB, the influx of 125 I-leptin still could be suppressed by excess unlabeled leptin, indicating persistence of its saturable transport system. When given a choice of either alcohol or control diet, even the alcohol-preferring B6 mice showed a significantly greater preference for the control liquid diet, and there was no evidence of BBB disruption or alterated leptin transport. Furthermore, acute alcohol intoxication induced by intraperitoneal injection of 20% alcohol did not result in BBB disruption or increased leptin permeation 4 h later. Thus, partial disruption of the BBB and increased permeation of leptin in both CD1 and B6 mice were only induced by chronic alcohol ingestion. The results showing increased leptin permeation across the BBB lead to the speculation that leptin may serve as a homeostatic feeding signal in these mice.

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Section: Discussionmentioning

confidence: 99%

Increased Leptin Permeation across the Blood–Brain Barrier after Chronic Alcohol Ingestion

Pan

Barron

Hsuchou

et al. 2007

Neuropsychopharmacol

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“…When DBA/2 J mice were injected systemically, the D1R partial agonist SKF-82958 showed no effect on sensitization to the locomotorstimulating effects of ethanol (Broadbent et al 2005). Although the i.p.…”

Section: Dopamine D1 Receptor and Voluntary Ethanol Consumptionmentioning

confidence: 99%

Involvement of nucleus accumbens dopamine D1 receptors in ethanol drinking, ethanol-induced conditioned place preference, and ethanol-induced psychomotor sensitization in mice

Bahí

Dreyer

2012

Psychopharmacology

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Rationale Dopamine D1 receptor (D1R) signaling has been associated to ethanol consumption and reward in laboratory animals. Objectives Here, we hypothesize that this receptor, which is located within the nucleus accumbens (NAc) neurons, modulates alcohol reward mechanisms. Methods To test this hypothesis, we measured alcohol consumption and ethanol-induced psychomotor sensitization and conditioned place preference (CPP) in mice that received bilateral microinjections of small interference RNA (siRNA)-expressing lentiviral vectors (LV-siD1R) producing D1R knock-down. The other group received control (LV-Mock) viral vectors into the NAc. Results There were no differences in the total fluid consumed and also no differences in the amount of ethanol consumed between groups prior to surgery. However, after surgery, the LV-siD1R group consumed less ethanol than the control group. This difference was not associated to taste neophobia. In addition, results have shown that downregulation of endogenous D1R using viral-mediated siRNA in the NAc significantly decreased ethanol-induced behavioral sensitization as well as acquisition, but not expression, of ethanol-induced place preference.Conclusions We conclude that decreased D1R expression into the NAc led to reduced ethanol rewarding properties, thereby leading to lower voluntary ethanol consumption. Together, these findings demonstrate that the D1 receptor pathway within the NAc controls ethanol reward and intake.

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“…Didone et al have reported a significant positive correlation between sensitization of dopaminergic neuronal activity and behavioral sensitization induced by EtOH. 18) Because the process of sensitization to the effects of a drug is affected by the administered dose, dosing interval, and administration term, [19][20][21][22][23] we also examined EtOH-induced locomotor sensitization under different levels of illumination in the CPP box, the dependence of EtOH-induced associative learning on the administered dose, and differences in the sensitizing effects of continuous and intermittent EtOH administration.…”

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confidence: 99%

Factors Affecting Ethanol-Induced Conditioned Place Preference and Locomotor Sensitization in Mice

Shimizu

Oki

Mitani

et al. 2015

Biological & Pharmaceutical Bulletin

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The rewarding effects of alcohol can lead to progressively heavier and more frequent drinking. Since studies of reward have mainly focused on responses to higher alcohol doses, the relations between reward and moderate/sustained alcohol exposure remain unknown. Our objective was to evaluate factors affecting the reward value of low alcohol doses and risk factors for increasing alcohol doses due to reward progression caused by alcohol exposure patterns. We thus performed conditioned place preference (CPP) and ethanol (EtOH)-induced locomotor sensitization tests in mice. Low-dose EtOH (0.5 or 1 g/kg twice/week)-induced CPP was stronger than that produced by saline control treatment, but the effect decreased with increasing numbers of conditioning trials. Moderate-dose/long-term EtOH exposure induced a weaker CPP than high-dose/short-term EtOH (2 g/kg twice/week) exposure with the same total EtOH dose (8 g/kg/experiment). Acamprosate calcium, an anti-relapse drug, preclusively reduced EtOH-induced CPP. EtOH induced CPP and locomotor sensitization in black but not white chamber, although the initial preference and the basal locomotion in each chamber were equal. Therefore the brightness of the chamber had an effect on EtOHinduced sensitization. Moreover, additional studies indicated that EtOH-induced locomotor sensitization also depends on the dose but not the administration interval. Paired associative learning with EtOH exposure is a potent factor influencing the level of reward produced by EtOH. Moreover, exposure to high doses of alcohol, even on an intermittent schedule, carries a higher risk of addiction than exposure to moderate doses over longer periods.Key words moderate alcohol (ethanol: EtOH); conditioned place preference (CPP); reward; sensitization; paired associative learning Alcohol abuse is associated with serious physical and psychiatric illnesses, financial hardships, familial dysfunction, and violence, all of which place a substantial burden on society. Heavy alcohol consumption and long-term drinking increase the risk of alcohol-related diseases such as liver cirrhosis, cancer, pancreatitis, and depression. 1,2) In response, the World Health Organization (WHO) recently approved a Global Strategy to Reduce Harmful Use of Alcohol urging all countries to strengthen national responses to public health problems caused by alcohol use.3) In Japan, 6.45 million people suffer from alcohol-related problems, with an estimated annual economic loss of 4.15 trillion yen associated with alcohol. 4) In December 2013, the Basic Act on Measures against Alcohol-related Health Harm was enacted in Japan, promoting education about drinking in moderation to prevent alcoholrelated problems.Regular consumption of alcohol increases the propensity for addiction because of the rewarding effects of alcohol. Thus, many casual drinkers gradually increase total alcohol consumption, which becomes habitual over time. Although many studies in rodents have been conducted on chronic drinking and reward, 5-7) previous studies have ma...

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Role of dopamine in behavioral sensitization to ethanol in DBA/2J mice

Cited by 35 publications

References 35 publications

Increased Leptin Permeation across the Blood–Brain Barrier after Chronic Alcohol Ingestion

Increased Leptin Permeation across the Blood–Brain Barrier after Chronic Alcohol Ingestion

Involvement of nucleus accumbens dopamine D1 receptors in ethanol drinking, ethanol-induced conditioned place preference, and ethanol-induced psychomotor sensitization in mice

Factors Affecting Ethanol-Induced Conditioned Place Preference and Locomotor Sensitization in Mice

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