Sure! Thanks for the question.
For people who don’t know, all addictions are thought to act on the mesolimbic dopamine system (the reward system), which includes the ventral tegmental area (VTA) which releases dopamine, Nucleus Accumbens (on which the dopamine acts), and prefrontal cortex. Drugs of addiction, including alcohol, act on this system to increase dopamine, a neurotransmitter which can produce that good feeling that drives addiction (as a simple explanation). Alcohol isn’t as obvious as, say, cocaine which increases dopamine by blocking the dopamine transporter. Unlike other drugs, alcohol doesn’t seem to act on a specific receptor in the brain (at least that we have found thus far). Instead, it appears that alcohol may act on other effectors of the dopaminergic system, such as GABA, glutamate, and serotonin. These systems seem to cause neuroadaptive changes that upon withdrawal of alcohol can cause dopaminergic decrease and withdrawal symptoms. For instance, alcohol seems to inhibit glutamate receptors, as shown in the image above. Chronic use will cause chronic inhibition of these receptors, which will modulate postsynaptic responses and protein composition (i.e. it could change the number of receptors) to glutamate. These neurons are located throughout the mesolimbic system. Thus, since their response is changed, the way the mesolimbic system works will also change. It’s been found in rats that chronic ethanol (alcohol) will increase sensitivity to glutamate and withdrawal from ethanol can cause hyperexcitability of the brain which leads to things like seizures. Anyway, to be clear, the whole effect of alcohol on the mesolimbic dopamine system is very complex, and it seems like alccohol may mediate the activity in this system through other neurotransmitters (aside from dopamine), but still have an effect on the dopaminergic system. Hope this helps!