Alcohol-induced changes in brain functions can lead to disordered cognitive functioning, disrupted emotions and behavioral changes. Moreover, these brain changes are important contributing factors to the development of alcohol use disorders, including acute intoxication, long-term misuse and dependence. While drinking initially boosts a person’s dopamine levels, the brain adapts to the dopamine overload with continued alcohol use. It produces less of the neurotransmitter, reducing the number of dopamine receptors in the body and increasing dopamine transporters, which carry away the excess dopamine. Researchers are investigating whether drugs that normalize dopamine levels in the brain might be effective in reducing alcohol cravings and treating alcoholism.
There are also notable differences in dopamine response between casual drinkers and heavy drinkers. In casual or light drinkers, alcohol consumption typically results in a predictable increase in dopamine release, contributing to the pleasurable effects drug addiction treatment of drinking. However, in heavy drinkers or individuals with alcohol use disorders, the dopamine system can become dysregulated. Genetic factors play a significant role in influencing alcohol’s impact on dopamine.
While the anxiolytic effect of alcohol is due in part to its effects on various neurotransmitter systems (e.g., GABA or glutamate), increased DA release also contributes to reduced anxiety and mediates the reinforcing properties of ethanol. There are likely multiple mechanisms by which acute ethanol can enhance DA release that involve direct effects of ethanol on intrinsic excitability of VTA DA neurons. Acute ethanol itself has direct effects on DA VTA neurons that result in higher firing frequency and increased excitability. Under baseline conditions in the absence of acute alcohol, DA neurons in the VTA fire in spontaneous, low-frequency pacemaker-like bursts that occur in the absence of outside synaptic inputs. The pacemaker frequency is set by an inward cation current, termed Ih, that is activated by hyperpolarization (Neuhoff, Neu, Liss, & Roeper, 2002). Acutely, ethanol enhances this current resulting in increased firing and likely enhancement of dopamine release in target regions such as the NAcc core (NAccC) and PFC (Brodie & Appel, 1998; Okamoto, Harnett, & Morikawa, 2006).
Understanding these individual variations is crucial for developing personalized approaches to alcohol use prevention and treatment. It highlights the need for tailored interventions that take into account a person’s unique genetic makeup, drinking history, and personal circumstances. Dopamine is released in response to rewarding stimuli, creating feelings of pleasure and satisfaction. This release encourages us to repeat behaviors that led to the reward, which is essential for survival-related activities like eating and reproduction. However, this same mechanism can also contribute to the development of addictive behaviors.
In addition, fast dopamine release events (dopamine transients) commence at the onset of a conditioned cue 18, 19. Pavlovian conditioned responses to alcohol cues in rodents provide a model of alcohol AB that allows direct measurements and mechanistic manipulations of the neural circuitry underlying AB 20,21,22. Taken together, preclinical evidence indicates a key role for dopaminergic pathways in mediating does alcohol release dopamine responses to alcohol-related cues 23,24,25. Moreover, work in non-human primates highlights a role for the prefrontal cortex in reward signaling 26, and human fMRI studies show that prefrontal cortex drives phasic cue responses in the VTA 27, 28. However, the dopaminergic circuitry mediating AB to alcohol cues in humans––and the extent to which this circuitry overlaps with the circuitry mediating conditioned responses to non-drug rewards––remains unclear. Chronic alcohol-induced disruption of dopamine modulation of prefrontal activity plays a major role in the cognitive dysfunction that persists well into abstinence and may contribute to the high probability of relapse in dependent individuals.
Similarly, Kiianmaa and colleagues28 found no differential increase of extracellular DA concentration in the NAc between AA and ANA rats after microdialysis of ethanol. These varying results may be due to the use of different animal models or different research protocols. As it turns out, the complex world of human brain chemistry — particularly the world of a potent neurotransmitter known as dopamine — holds the key to these questions. We may have heard dopamine praised as a “feel-good” chemical, but does alcohol increase dopamine or lower it? Researchers at McGill University in Canada performed positron emission tomography (PET) brain scans on 26 social drinkers and noted a “distinctive brain response” in the higher-risk subjects after they consumed three alcoholic drinks.
As a result, people with an alcohol addiction may consume even more alcohol in an unconscious effort to boost their dopamine levels and get that spark back. However, when it comes to dopamine levels and addictive substances, alcohol behaves somewhat differently than other substances or pharmaceuticals. While we’ve discussed the general effects of alcohol on dopamine, it’s crucial to understand that these effects can vary significantly from person to person. Several factors contribute to these individual variations, including genetics, tolerance, and drinking patterns. “We believe that mice with less KCNK13 in the VTA drank more alcohol in order to achieve the same ‘reward’ from alcohol as normal mice, presumably because alcohol was triggering the release of less dopamine in their brains,” Brodie said.
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