People with family history of alcoholism release more dopamine in expectation of alcohol: A new study in Biological Psychiatry: Cognitive Neuroscience and Neuroimaging investigates the brain chemistry of alcohol exposure in people with a range of risk for alcohol use disorder ScienceDaily

Researchers are investigating whether drugs that normalize dopamine levels in the brain might be effective in reducing alcohol cravings and treating alcoholism. To test the effects of weakening D2 receptors in the brain, the researchers first conditioned mice to resemble alcoholics by putting them through a cycle of binging and recovery. Not surprisingly, they saw that D2 receptors showed signs of decreased activity, indicating that the mice felt a greater compulsion to drink alcohol. They then manipulated the two receptors, and watched to see how the mice reacted. Strengthening the activity of the D2 receptors caused the mice to drink less, while strengthening the D1 receptors caused them to drink more, and vice versa.

Why do people with ADHD drink?

Some people with ADHD may have trouble avoiding alcohol or binge drinking due to impulsiveness. Others might believe alcohol can quell their restlessness and calm them down. Because those with ADHD tend to seek rewards, they may also turn to alcohol for its initial feel-good effects.

Indeed, a major role for nAChRs on dopamine terminals in regulating dopamine release has been demonstrated in rodents [53,54,55,56,57]. This disynaptic mechanism involves acetylcholine released from cholinergic interneurons activating nAChRs on dopamine axons to induce dopamine release. Thus, any changes to cholinergic signaling in striatum might also influence changes in dopamine release.

Dopamine and Addiction Recovery: Here’s What You Should Know About the “Pleasure Chemical”

Furthermore, the specific neuronal circuitries were progressively mapped with major projections from the ventral tegmental area (VTA) to the nucleus accumbens (NAc, i.e. the ventral striatum), the prefrontal cortex (PFC) and amygdala. Collectively, this network of neurons was denominated the mesocorticolimbic dopamine system [12, 13]. In addition, there are dopamine projections from the VTA to the amygdala and the hippocampus, respectively, involved in reward associative learning and declarative memory formation [15, 17]. Given that treatment-seeking individuals with AUD invariably go through repeated periods of abstinence and relapse, it is important for animal models of AUD to incorporate this element into the experimental design as these abstinence periods may contribute to the neurobiology of AUD. Indeed, in rodent models, alcohol abstinence or withdrawal periods are often followed by enhanced rebound alcohol drinking, the alcohol deprivation effect [66]. This alcohol deprivation effect has also been observed in cynomolgus macaques [8].

Briefly, acute alcohol increases dopamine release across the striatum [14] primarily due to increased firing of midbrain dopaminergic neurons, an effect that may underlie the initial reinforcing properties of alcohol. In individuals that drink alcohol frequently, however, tolerance develops, and more alcohol is consumed. Concomitantly, adaptations in glutamatergic, GABAergic, and dopamine transmission occur [15] and greater or continued amounts of alcohol can result in allostatic changes to preserve normal brain function.

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These nAChR antagonists are limited in a clinical setting due to low blood–brain barrier permeability and an unfavourable side effect profile. The potential of nAChR’s as novel treatment target was revived with the marketing of the partial nAChR agonist varenicline as a smoking cessation agent. It has been shown that varenicline reduce alcohol intake and alcohol‐seeking behaviour in long‐term drinking rats [205] and modulate NAc dopamine after systemic administrations of alcohol alone and in combination with nicotine [206].

  • For example, different subpopulations of neurons in the striatum carry different dopamine receptors on their surfaces (Le Moine et al. 1990, 1991; Gerfen 1992).
  • As a result of this intense craving, conventional reinforcers (e.g., food, sex, family, job, or hobbies) lose their significance and have only a reduced impact on the drinker’s behavior.
  • On the other hand, local administration of the dopamine D2 receptor antagonist, sulpiride, into the anterior VTA did not alter alcohol nor sucrose intake in high‐alcohol‐preferring rats [142].
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Treatment with the dopamine D1 and D2 receptor antagonists SCH and L741,626 did not alter alcohol intake and preference. These findings are in agreement with the lack of effect of dopamine D1 and D2 receptor antagonists on voluntary alcohol consumption that has been reported previously (Brown et al. 1982; Goodwin et al. 1996; Silvestre et al. 1996). Importantly, the doses that reduced alcohol consumption often also decreased water intake, possibly reflecting a non-specific suppression of fluid intake or a more general impairment in motor activity (Linseman 1990; Hubbell et al. 1991; Dyr et al. 1993).


The selection of LD and HD was performed as previously described (Spoelder et al. 2015). Briefly, after 2 months of IAA, the rats were ranked based on the animals’ average alcohol intake per week and were assigned ranking scores. The weekly ranking scores were summed to calculate a total ranking score per rat. The rats within the lower and upper 25 % of the total ranking score range were designated as LD and HD, respectively.

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Alcohol dependence, family history, and D2 dopamine receptor function as neuroendocrinologically assessed with apomorphine

Some experiments found no difference in DA release in the NAc after intraperitoneal injection of ethanol between P and NP rats. For example, Yoshimoto and colleagues[11] and Gongwer and colleagues[23] found that although HAD and LAD rats differed in their basal level of alcohol and dopamine extracellular DA, they did not differ in CNS DA release after intraperitoneal injection of ethanol. Similarly, Kiianmaa and colleagues[28] found no differential increase of extracellular DA concentration in the NAc between AA and ANA rats after microdialysis of ethanol.

The mechanism of action is, however, not completely understood, and although in vitro studies indicate that OSU6162, like aripiprazole, acts as a partial agonist at D2 receptors [191, 192], behavioural studies have failed to demonstrate any intrinsic activity of the compound ([195]). Instead it has been suggested that OSU6162 produces functionally opposite effects by acting as an antagonist at both presynaptic autoreceptors and postsynaptic D2 receptors [189, 193–195]. Based on the hypothesis that OSU6162 can counteract both hyper‐ and hypo‐dopaminergic states, the compound has recently been evaluated in both animal models modulating alcohol‐mediated behaviours as well as in a placebo‐controlled human laboratory study in alcohol‐dependent patients.

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