Habitual alcohol seeking: modeling the transition from casual drinking to addiction

Abstract

The transition from goal-directed actions to habitual ethanol seeking models the development of addictive behavior that characterizes alcohol use disorders. The progression to habitual ethanol-seeking behavior occurs more rapidly than for natural rewards, suggesting that ethanol may act on habit circuit to drive the loss of behavioral flexibility. This review will highlight recent research that has focused on the formation and expression of habitual ethanol seeking, and the commonalities and distinctions between ethanol and natural reward-seeking habits, with the goal of highlighting important, understudied research areas that we believe will lead toward the development of novel treatment and prevention strategies for uncontrolled drinking.

Keywords: Addiction; Alcohol; Goal-directed behavior; Habit; Prefrontal cortex; Striatum.

Figure 1. Interactions between cognitive-behavioral processes that drive addiction

A number of models have proposed that the development of addiction, including alcohol use disorders, results from a transition from controlled behavior to uncontrolled drug seeking behavior. Innate risk for addictive behavior has been shown to be related to differences in impulsivity and cue-reactivity that exist prior to any drug exposure. These differences can initiate entry into the spiral toward addiction. Across alcohol exposure, dysregulation in limbic corticostriatal circuitry is expected to drive drug seeking, which acts to exacerbate deficits in behavioral control, ultimately facilitating the disease state. In addition to impulsivity and habitual reward seeking, addiction is characterized by compulsive behaviors. Compulsivity can be defined as either behaviors that persist despite or because of the negative consequences of drug taking. In other words, compulsive behaviors continue despite negative results of drug-taking or those negative results create an aversive state that can be relieved by ongoing drug-taking. Importantly, habit models a behavior that is more similar to the former in which drug-seeking is elicited by environmental stimuli rather than a desire to seek positive or negative reinforcement. Alternatively, the aversive state created by withdrawal may come to serve as an interoceptive stimulus, driving habitual reward seeking behavior. To our knowledge, the precise relationship between these behaviors has not been elucidated (though see Everitt, 2014; Koob & Volkow, 2010).

Fig 2. Neuroanatomical substrates of inflexible behavior

Blue regions represent those regions known to be required for the expression of goal-directed reward seeking. Red regions are required for the development or expression of stimulus-response habits. Midbrain DA signaling has been shown to play a role in both forms of behavior. The role for the nucleus accumbens in reward seeking is more complex. One possibility is that through the ‘ascending loops’ of projections from midbrain dopaminergic regions to striatal subregions, glutamate or DA signaling in the NAc shell can ultimately influence activity in dorsal striatum mediation of behavior. A role for the BLA has not yet been explicitly demonstrated, but is likely given its established role in stimulus-outcome learning and the encoding of outcome value. Only the dorsolateral striatum has been explicitly demonstrated to have the same role in habitual alcohol seeking as in habitual food seeking (Corbit et al., 2012).