Can dopamine receptors tell us who is more likely to develop an alcohol use disorder? Recovery Research Institute

When chronic heavy drinkers are intoxicated—and when they are withdrawing from alcohol intoxication—they can experience mood swings, diminished cognitive abilities, memory loss, and a decreased ability to learn. Let’s explore the immediate impact of alcohol on our dopamine levels and how it affects our motivation and reward system. Dopamine is a neurotransmitter, a chemical messenger that transmits signals between nerve cells in the brain.

Final Thoughts on Alcohol, Dopamine, and Motivation

Moreover, although increased serotonin levels at the synapses in the brain can moderate alcohol consumption, additional factors contribute to continued alcohol abuse. Consequently, SSRI’s cannot be recommended as the sole treatment for alcoholism. Preclinical evidence indicates an effect of NE pharmacotherapy both during acute withdrawal and in the maintenance of abstinence after chronic ethanol. Α2 agonists have shown further application in reducing operant self-administration of ethanol and reduce stress-induced reinstatement of ethanol seeking (Le et al. 2005).

Strategies to Support Dopamine Recovery After Quitting Alcohol

In short, the does alcohol decrease dopamine serotonin receptors in our central and peripheral nervous system get overwhelmed, leading to an all-out system overload. There’s also more of an effect on your brain and its development if you’re younger — one that can have a lasting impact. These effects can happen even after one drink — and increase with every drink you have, states Dr. Anand.

Does alcohol destroy brain cells?

Given the well-described link between GABA dysfunction in AUD and rTMS effects on the GABAergic system, it will be important to explore whether biomarkers of GABAergic functions can serve as mediators or moderators of rTMS efficacy. However, the studies mentioned above all evaluated the impact of positive modulation of the αx-GABAA receptor in the context of alcohol consumption or alcohol discrimination when the system is already sensitized to further GABAergic activity (Figure 1B – central panel). However, it remains unclear how such modulation would play in the context of withdrawal when the system is deficient in GABAergic regulation, which is, in turn, causing craving behaviors. Benzodiazepines (BZ) are allosteric modulators of the GABAA receptor that bind to the α1, 2, 3, 5, and γ subunits. They enhance the activity of GABA when binding at its receptor and are recommended in Halfway house managing acute alcohol withdrawal (Nelson et al., 2019), but not for the treatment of AUD itself.

• And before we know it, that morning cup of coffee can turn into two (or five, or the whole pot!).
• Dopamine is a neuromodulating compound that is released in the ventral tegmental area (VTA) and projects to the nucleus accumbens (NA) where it is acutely involved in motivation and reinforcement behaviours.
• Alcohol is converted by the liver to acetaldehyde and the resulting acetaldehyde is converted to acetate by aldehyde dehydrogenase acetate, which then enters the metabolic tricarboxylic acid (TCA) cycle.
• More recently, the EMA granted authorization also for nalmefene, a compound intended for the reduction of alcohol consumption in adults with alcohol dependence (EMA 2012).
• Raphe nuclei neurons extend processes to and dump serotonin onto almost the entire brain, as well as the spinal cord.

Does Alcohol Increase Dopamine

Another study by the global burden of disease (GBD) collaborative network reported a 1.5% global AUD prevalence in 2019, highlighting variabilities between countries (Castaldelli-Maia and Bhugra, 2022). Ethanol, the main active component of alcoholic beverages, is currently one of the most used psychoactive drugs on the market. Ethanol produces a state of anxiolysis and disinhibition, which is commonly sought after in social situations or in individuals with AUD (Gilman et al., 2008). While consumption patterns vary, the impact of ethanol at low doses on overall health remains unclear (Larsson et al., 2020; Zhao et al., 2023). A recent systematic meta-analysis of cohort studies showed no statistically significant protective effect of alcohol on all-cause mortality at low ethanol intakes (Zhao et al., 2023). Studies have highlighted that abstinence from alcohol has many health benefits, including improved sleep.

The main inhibitory neurotransmitter in the brain is gamma-aminobutyric acid (GABA). Acting through a receptor subtype called GABAA, GABA leads to a state of sedation and decreased anxiety. Sedative medications such as the benzodiazepines (e.g., Valium®) also act at the GABAA receptor. Some reports suggest that short-term alcohol exposure increases the inhibitory effect of GABAA receptors (Mihic and Harris 1995).

• SERT availability was measured in vivo with single photon emission computed tomography and (123) I-labeled 2-((2-((dimethyl-amino) methyl) phenyl) thio)-5-iodophenylamine in the midbrain, thalamus and striatum.
• Thus, these GABAA receptor subunit composition changes are a mechanism underlying the behavioral changes after chronic ethanol exposure, which leads to additional risks of developing dependence.
• Mindfulness practices, meditation, and cognitive behavioral therapy (CBT) can also help regulate mood and improve dopamine function by reinforcing healthier reward mechanisms.

Also importantly, the findings showing no association between dopamine receptors and later hazardous drinking were similar both for individuals with and without a family history of substance use disorder. Baclofen is only approved for the treatment of alcohol withdrawal in France (Garbutt, 2019). Despite multiple trials supporting its efficacy in reducing the risk of relapse and increasing abstinence days (Agabio et al., 2023), its efficacy remains controversial, and systematic reviews consider the evidence of its efficacy insufficient (Jonas et al., 2014).