Figure 1.

The neuroadaptive model of craving. This model proposes that chronic alcohol exposure leads to changes in brain cell function (i.e., sensitization, or neuroadaptation) that are expressed as changes in the activity of various brain chemicals (i.e., neurotransmitters), such as dopamine, glutamate, gamma-aminobutyric acid (GABA), and endogenous opioids. Neuroadaptation can contribute to certain characteristics of alcohol dependence, such as withdrawal, and to the development of a reward memory—that is, the memory of the importance of alcohol or alcohol-related stimuli to the drinker’s well-being. During initial abstinence, when alcohol withdrawal may occur, neuroadaptation leads to an imbalance in brain function, which results in subjective feelings of discomfort and, subsequently, craving. During prolonged abstinence, situations or stimuli previously associated with alcohol consumption may activate the reward memory, thereby also inducing craving. Craving, in turn, may result in relapse to drinking. Stress, which on a chemical level is mediated by the neurotransmitter serotonin, can enhance neuroadaptation as well as trigger the reward memory.