Voluntary Ethanol Intake Increases Extracellular Acetylcholine Levels in the Ventral Tegmental Area in the Rat

Larsson, Åsa; Edström, Lena; Svensson, Lennart; Söderpalm, Bo; Engel, Jörgen A.

doi:10.1093/alcalc/agh180

Cited by 121 publications

(100 citation statements)

References 65 publications

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“…Consistent with this observation, Landgren et al (2009) report an interesting association with CHRNA4 and obesity, particularly within heavy alcohol users. This result may not be surprising given that the cholinergic dopaminergic reward effect seen with alcohol can also be seen with food (Larsson et al, 2005). Associations between CHRNA4 and ADHD (Todd et al, 2002) and cognitive attention (Greenwood et al, 2012), may suggest yet other mechanisms underlying the relationship between CHRNA4 and frequency of binging.…”

Section: Discussionmentioning

confidence: 93%

Association of the CHRNA4 Neuronal Nicotinic Receptor Subunit Gene with Frequency of Binge Drinking in Young Adults

Coon

Piasecki

Cook³

et al. 2014

Alcoholism Clin & Exp Res

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Background Binge drinking is responsible for over half of all alcohol-related deaths, and results in significant health and economic costs to individuals and society. Knowledge of genetic aspects of this behavior, particularly as it emerges in young adulthood, could lead to improved treatment and prevention programs. Methods We have focused on the association of variation in neuronal nicotinic receptor subunit genes (CHRNs) in a cohort of 702 Hispanic and non-Hispanic White young adults who are part of the Social and Emotional Contexts of Adolescent Smoking Patterns (SECASP) study. Fifty-five single nucleotide polymorphisms covering the variation in five CHRNs (CHRNA4, CHRNB2, CHRNA2, CHRNB3A6 and CHRNA5A3B4) were studied. Results Frequency of binge drinking and other correlated alcohol consumption measures were significantly associated with SNPs in CHRNA4 (p-values ranged from 0.0003 to 0.02), but not with SNPs in other CHRNs. This association was independent of smoking status in our cohort. Conclusions Variants in CHRNA4 may contribute to risk for binge drinking in young adults in this cohort. Results will need to be confirmed in independent samples.

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Section: Discussionmentioning

confidence: 93%

Association of the CHRNA4 Neuronal Nicotinic Receptor Subunit Gene with Frequency of Binge Drinking in Young Adults

Coon

Piasecki

Cook³

et al. 2014

Alcoholism Clin & Exp Res

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“…This reward link is activated by natural as well as chemical reinforcers, as reviewed previously (Larsson and Engel 2004). Involvement of this reward link in druginduced as well as natural reward has been implied, thus food as well as alcohol intake increases the ventral tegmental acetylcholine levels as well as accumbal dopamine levels (Hernandez and Hoebel 1988;Larsson et al 2005;Rada et al 2000). GHS-R1A is expressed in the LDTg (Guan et al 1997), specifically on cholinergic cells , suggesting that ghrelin may have direct effects in this reward node.…”

Section: The Central Ghrelin Signalling System Integrates With a Key mentioning

confidence: 85%

“…These data are verified in clinical tests; thus blocking these subtypes, by using varenicline, reduces the intake of alcohol in heavy drinking smokers (McKee et al 2009) and one haplotype of the 6* gene is associated with heavy alcohol use ). Furthermore, it has been shown that excessive alcohol intake in rats consuming alcohol for a long period of time causes a release of acetylcholine in the VTA followed by an increase in accumbal dopamine levels, showing that alcohol like ghrelin activates the cholinergicdopaminergic reward link (Larsson et al 2005). Taken together, there appears to be neurochemical analogies and overlaps between ghrelin and alcohol, where the cholinergic-dopaminergic reward link is the common denominator.…”

Section: The Central Ghrelin Signalling System Integrates With a Key mentioning

confidence: 96%

The role of the central ghrelin system in reward from food and chemical drugs

Dickson

Egecioglu

Landgren

et al. 2011

Molecular and Cellular Endocrinology

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Here we review recent advances that identify a role for the central ghrelin signalling system in reward from both natural rewards (such as food) and artificial rewards (that include alcohol and drugs of abuse). Whereas ghrelin emerged as a stomach-derived hormone involved in energy balance, hunger and meal initiation via hypothalamic circuits, it now seems clear that it also has a role in motivated reward-driven behaviours via activation of the so-called "cholinergic-dopaminergic reward link". This reward link comprises a dopamine projection from the ventral tegmental area (VTA) to the nucleus accumbens together with a cholinergic input, arising primarily from the laterodorsal tegmental area. Ghrelin administration into the VTA or LDTg activates the "cholinergicdopaminergic" reward link, suggesting that ghrelin may increase the incentive value of motivated behaviours such as reward-seeking behaviour ("wanting" or "incentive motivation"). Further, direct injection of ghrelin into the brain ventricles or into the VTA

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“…Alcohol targets components of the mesolimbic dopamine system (Larsson & Engel 2004;Vengeliene et al 2008;Soderpalm, Lof, & Ericson 2009), which is involved in the expression of its reinforcing properties (Adinoff 2004). Beyond the mesolimbic dopamine system, which includes dopamine projections from the ventral tegmental area (VTA) to nucleus accumbens (NAc) (Koob & Bloom 1988;Kelley & Berridge 2002), recent studies show that alcohol activates the cholinergic inputs from the laterodorsal tegmental nucleus (LDTg) (Larsson et al 2005).…”

Section: Introductionmentioning

confidence: 99%

Activation of amylin receptors attenuates alcohol‐mediated behaviours in rodents

2018

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Alcohol expresses its reinforcing properties by activating areas of the mesolimbic dopamine system, which consists of dopaminergic neurons projecting from the ventral tegmental area to the nucleus accumbens. The findings that reward induced by food and addictive drugs involve common mechanisms raise the possibility that gut-brain hormones, which control appetite, such as amylin, could be involved in reward regulation. Amylin decreases food intake, and despite its implication in the regulation of natural rewards, tenuous evidence support amylinergic mediation of artificial rewards, such as alcohol. Therefore, the present experiments were designed to investigate the effect of salmon calcitonin (sCT), an amylin receptor agonist and analogue of endogenous amylin, on various alcohol-related behaviours in rodents. We showed that acute sCT administration attenuated the established effects of alcohol on the mesolimbic dopamine system, particularly alcohol-induced locomotor stimulation and accumbal dopamine release. Using the conditioned place preference model, we demonstrated that repeated sCT administration prevented the expression of alcohol's rewarding properties and that acute sCT administration blocked the reward-dependent memory consolidation. In addition, sCT pre-treatment attenuated alcohol intake in low alcohol-consuming rats, with a more evident decrease in high alcohol consumers in the intermittent alcohol access model. Lastly, sCT did not alter peanut butter intake, blood alcohol concentration and plasma corticosterone levels in mice. Taken together, the present data support that amylin signalling is involved in the expression of alcohol reinforcement and that amylin receptor agonists could be considered for the treatment of alcohol use disorder in humans.

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Voluntary Ethanol Intake Increases Extracellular Acetylcholine Levels in the Ventral Tegmental Area in the Rat

Cited by 121 publications

References 65 publications

Association of the CHRNA4 Neuronal Nicotinic Receptor Subunit Gene with Frequency of Binge Drinking in Young Adults

Association of the CHRNA4 Neuronal Nicotinic Receptor Subunit Gene with Frequency of Binge Drinking in Young Adults

The role of the central ghrelin system in reward from food and chemical drugs

Activation of amylin receptors attenuates alcohol‐mediated behaviours in rodents

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